Hand disinfection: a comparison of various agents in laboratory and ward studies

The efficacy of 14 handwashing or disinfectant preparations was compared in laboratory tests on staff volunteers. The test organism, Escherichia coli, was applied to the fingertips and log reductions (LR) were measured following treatment with the test agent and control preparations (70% isopropanol and non-medicated bar soap). Alcoholic preparations, particularly n-propanol and isopropanol were the most effective showing LRs of 3.1-3.8. Chlorhexidine (LR 2.9) and povidone-iodine detergent preparations were significantly more effective than non-medicated soap (LR 2.1), but triclosan products were not. In addition the residual effect of several of these formulations was assessed after 10 applications by comparing the survival of E. coli on the fingertips over a 32-min period. This number of handwashes compares favourably with those recorded during an 8 h nursing shift. Chlorhexidine-detergent consistently showed the best residual activity. Alcoholic formulations showed little or no residual effect. The survival studies show that on the whole gram-positive organisms (Staphylococcus aureus and Candida albicans) survive better on the skin than Gram-negative bacilli (GNB). However, it would seem that GNB which are considered to be residents (Acinetobacter calcoaceticus and Enterobacter spp.) survive much better than many other GNB (Pseudomonas aeruginosa, E. coli and Proteus vulgaris). The Klebsiella species varied in survival times. Random sampling of ward staff hands showed that contamination with S. aureus and GNB was greater in dermatological and general wards than in an isolation unit, where handwashing or disinfection was carried out after every patient contact. No cross-infection occurred in the isolation ward during periods of study in which 70% alcohol, chlorhexidine-detergent and non-medicated soap were used.     

Neuropathy and the vascular-bone axis in diabetes: lessons from Charcot osteoarthropathy

Emerging evidence from the last two decades has shown that vascular calcification (VC) is a regulated, cell-mediated process orchestrated by vascular smooth muscle cells (VSMCs) and that this process bears many similarities to bone mineralization. While many of the mechanisms driving VSMC calcification have been well established, it remains unclear what factors in specific disease states act to promote vascular calcification and in parallel, bone loss. Diabetes is a condition most commonly associated with VC and bone abnormalities. In this review, we describe how factors associated with the diabetic milieu impact on VSMCs, focusing on the role of oxidative stress, inflammation, impairment of the advanced glycation end product (AGE)/receptor for AGE system and, importantly, diabetic neuropathy. We also explore the link between bone and VC in diabetes with a specific emphasis on the receptor activator of nuclear factor κβ ligand/osteoprotegerin system. Finally, we describe what insights can be gleaned from studying Charcot osteoarthropathy, a rare complication of diabetic neuropathy, in which the occurrence of VC is frequent and where bone lysis is extreme.     

The Colonic Microbiota and Colonic Disease

The colonic ecosystem differs from that in the proximal gut in several important respects. The colonic microbiota represents the largest population of microbes colonizing humans from birth. Constraints on bacterial numbers, composition, and interaction with the host involve not only the innate and acquired immune system, but also the colonic mucin structure. While the microbiota provides beneficial protective, trophic, nutritional, and metabolic signals for the host, it may become a risk factor for disease depending on context and host susceptibility. Technological advances including DNA-based high-throughput compositional analysis have linked changes in the indigenous microbiota with several human diseases. In some instances, these findings have the potential to serve as new biomarkers of risk of disease. In this overview, recent advances are focused upon in relation to irritable bowel syndrome, inflammatory bowel disease, and colon cancer. The possibility that the therapeutic solution to some of these disorders may reside within the microbiota will also be addressed.     

Annexin‐A1 identified as the oral epithelial cell anti‐Candida effector moiety

Innate and adaptive immunity are considered critical to protection against mucosal candidal infections. Among innate anti‐Candida mechanisms, oral and vaginal epithelial cells have antifungal activity. The mechanism is fungistatic, acid‐labile and includes a requirement for cell contact by intact, but not necessarily live, epithelial cells. The purpose of this study was to use the acid‐labile property to further characterize the effector moiety. Surface material extracted from phosphate‐buffered saline (PBS) ‐treated, but not acid‐treated, epithelial cells significantly inhibited the growth of Candida blastoconidia in a dose‐dependent manner which was abrogated by prior heat and protease treatment. Proteins extracted from PBS‐treated cells bound blastoconidia and hyphae more intensely than those from acid‐treated cells. Proteins from PBS‐treated cells eluted from Candida revealed two unique bands of approximately 33 and 45 kDa compared with acid‐treated cells. Mass spectrometry identified these proteins as Annexin‐A1 and actin, respectively. Oral epithelial cells stained positive for Annexin‐A1, but not actin. Western blots showed reduced Annexin‐A1 in proteins from acid‐treated epithelial cells compared with those from PBS‐treated epithelial cells. Lastly, it was demonstrated that immunoprecipitation of Annexin‐A1 from proteins extracted from PBS‐treated oral epithelial cells resulted in abrogation of inhibitory activity. Taken together, these results indicate that Annexin‐A1 is a strong candidate for the epithelial cell anti‐Candida effector protein.     

Contemporary surgery of biliary atresia

The etiology of biliary atresia is not due to a congenital malformation but rather to a continuing process beginning in utero that affects not only the extrahepatic biliary ducts but also the intrahepatic parenchyma. Over the last decade, the outlook for patients who were previously felt to be uncorrectable has been significantly improved by Kasai's operation. Successful biliary reconstruction depends on early diagnosis and treatment (before three months of age). The essentials of hepatic portoenterostomy consist of excision of the entire extrahepatic duct structure with anastomosis of an intestinal conduit to the area of the transected duct at the liver hilus. After operation, many patients experience complications, including cholangitis, portal hypotension, and vitamin deficiencies. Despite these difficulties, growth and development continue on a relatively normal course, and long-term survival has been accomplished in many children. For those in whom biliary drainage is not achieved or with significant parenchymal damage, liver transplantation should be considered as part of ongoing care.