Profiling of nosocomial infection in hepatic patients

Background: Nosocomial infection (NCI) is a problem with global concern due to increasing morbidity and mortality in hospitalized patients. Chronic liver disease increases the chance of NCI by suppressing cell and antibody mediated immunity. Aim: We aimed in this study to visualize the problem of NCI in hepatic patients regarding organisms causing it, pattern of resistance and possible device associated with its existence. Methods: End stage chronic hepatitis C patients who admitted to the National Liver Institute Hospital, Menoufia University, were enrolled in this observational study. Different samples from alleged sites further processed by conventional culture and sensitivity techniques and confirmed by VITEK2C2 system. Antibiotic resistance pattern of isolates was assessed.  Pan drug resistance  (PDR) Acinetobacter baumannii to Omp A, bap, and Csu E virulence genes was further processed by Multiplex PCR.  Results: Gram- negative pathogens were significantly higher in CAUTI. The most predominant nosocomial organism was Pseudomonas aeruginosa which represent 19% (32 from 168), followed by Staph aureus that account for 17.86% (30 from 168), Acinetobacter baumannii signify 14.2%, Klebsiella pneumonia form 11.9%. MDR represents 123 isolates from 168 with 73.2% percentage, while XDR represents 23.8% of total isolates.  Pan drug resistance Acinetobacter baumannii represents 5 from 24 isolates. It was associated with CAUTI and CLBSI but non-significant. 4 PDR isolates show Prescence of Omp A, Csu E, and bap biofilm forming genes. Conclusions: MDR NCI in hepatic patients need more attention regarding rational use of antibiotics especially with appearance of PDR Acinetobacter baumannii carrying Omp A, Csu E, and bap biofilm forming genes

Spent Culture Medium from Virulent Borrelia burgdorferi Increases Permeability of Individually Perfused Microvessels of Rat Mesentery

Lyme disease is a common vector-borne disease caused by the spirochete Borrelia burgdorferi (Bb), which manifests as systemic and targeted tissue inflammation. Both in vitro and in vivo studies have shown that Bb-induced inflammation is primarily host-mediated, via cytokine or chemokine production that promotes leukocyte adhesion/migration. Whether Bb produces mediators that can directly alter the vascular permeability in vivo has not been investigated. The objective of the present study was to investigate if Bb produces a mediator(s) that can directly activate endothelial cells resulting in increases in permeability in intact microvessels in the absence of blood cells.The effects of cell-free, spent culture medium from virulent (B31-A3) and avirulent (B31-A) B. burgdorferi on microvessel permeability and endothelial calcium concentration, [Ca(2+)](i), were examined in individually perfused rat mesenteric venules. Microvessel permeability was determined by measuring hydraulic conductivity (Lp). Endothelial [Ca(2+)](i), a necessary signal initiating hyperpermeability, was measured in Fura-2 loaded microvessels. B31-A3 spent medium caused a rapid and transient increase in Lp and endothelial [Ca(2+)](i). Within 2-5 min, the mean peak Lp increased to 5.6+/-0.9 times the control, and endothelial [Ca(2+)](i) increased from 113+/-11 nM to a mean peak value of 324+/-35 nM. In contrast, neither endothelial [Ca(2+)](i) nor Lp was altered by B31-A spent medium.A mediator(s) produced by virulent Bb under culture conditions directly activates endothelial cells, resulting in increases in microvessel permeability. Most importantly, the production of this mediator is associated with Bb virulence and is likely produced by one or more of the 8 plasmid(s) missing from strain B31-A

Preparation and molecular modeling of radioiodopropranolol as a novel potential radiopharmaceutical for lung perfusion scan

Objective: Development of easy method for radioiodination of propranolol with high percent labeling yield for the purpose of lung perfusion imaging.Methods: Radioidination of propranolol was achieved using 125I via electrophilic substitution under the oxidative conditions of cholramine-T (CAT). All factors affecting the labeling procedure and labeling yield were studied. Paper electrophoresis and HPLC were performed to determine the radiochemical yield and purity of the 125I-propranolol. Molecular modeling and docking studies were performed to ensure the binding of the newly obtained 125I-propranolol to beta-2 (β2) adrenergic receptor.Results: Radioiodination of propranolol has been successfully achieved with high labeling yield (93.7 ± 0.81% ) . 125I-propranolol was stable for 24 h when kept in dark at ambient temperature. Biodistribution studies showed lung uptake of 21.60 ± 0.03% injected dose/g  (%ID/g) at 30 min post-injection. Molecular modeling confirmed that radioiodination did not affect the binding of propranolol to β2- receptor.Conclusion: Iodopropranolol can be considered as good potential lung perfusion agent as suggested by the results of biodistribution and molecular modeling studies