Interventions to improve hand hygiene compliance in patient care

Four studies met the criteria for the review: two from the original review and two from the update. Two studies evaluated simple education initiatives, one using a randomized clinical trial design and the other a controlled before and after design. Both measured hand hygiene compliance by direct observation. The other two studies were both interrupted times series studies. One study presented three separate interventions within the same paper: simple substitutions of product and two multifaceted campaigns, one of which included involving practitioners in making decisions about choice of hand hygiene products and the components of the hand hygiene program. The other study also presented two separate multifaceted campaigns, one of which involved application of social marketing theory. In these two studies follow-up data collection continued beyond 12 months, and a proxy measure of hand hygiene compliance (product use) was recorded. Microbiological data were recorded in one study. Hand hygiene compliance increased for one of the studies where it was measured by direct observation, but the results from the other study were not conclusive. Product use increased in the two studies in which it was reported, with inconsistent results reported for one initiative. MRSA incidence decreased in the one study reporting microbiological data

MyD88 Dependent Signaling Contributes to Protective Host Defense against Burkholderia pseudomallei

Background: Toll-like receptors (TLRs) have a central role in the recognition of pathogens and the initiation of the innate immune response. Myeloid differentiation primary-response gene 88 (MyD88) and TIR-domain-containing adaptor protein inducing IFNb (TRIF) are regarded as the key signaling adaptor proteins for TLRs. Melioidosis, which is endemic in SE-Asia, is a severe infection caused by the gram-negative bacterium Burkholderia pseudomallei. We here aimed to characterize the role of MyD88 and TRIF in host defense against melioidosis. Methodology and Principal Findings: First, we found that MyD88, but not TRIF, deficient whole blood leukocytes released less TNFa upon stimulation with B. pseudomallei compared to wild-type (WT) cells. Thereafter we inoculated MyD88 knockout (KO), TRIF mutant and WT mice intranasally with B. pseudomallei and found that MyD88 KO, but not TRIF mutant mice demonstrated a strongly accelerated lethality, which was accompanied by significantly increased bacterial loads in lungs, liver and blood, and grossly enhanced liver damage compared to WT mice. The decreased bacterial clearance capacity of MyD88 KO mice was accompanied by a markedly reduced early pulmonary neutrophil recruitment and a diminished activation of neutrophils after infection with B. pseudomallei. MyD88 KO leukocytes displayed an unaltered capacity to phagocytose and kill B. pseudomallei in vitro. Conclusions: MyD88 dependent signaling, but not TRIF dependent signaling, contributes to a protective host respons