We read with interest the recent review by Tilg et al ,1 which summarised the role of microbiota in liver diseases and pointed out that a causal link with systemic inflammation has still not been established. This letter fills in this gap and provides an analysis of the circulating microbiota in portal vein as the link between gut and liver. The access to portal circulation is possible during the implantation of a transjugular intrahepatic portosystemic shunt (TIPS). Therefore, we characterised the circulating microbiome in portal vein (first venous outflow in gut–liver axis), liver outflow, central venous blood and peripheral venous blood from seven patients with decompensated liver cirrhosis receiving TIPS for either variceal bleeding (n=3) or refractory ascites (n=4) (mean Model for End-stage Liver Disease (MELD) 8.4 (range 6–13), Child-Pugh-Score (CHILD) A: n=4, CHILD B: n=3) (figure 1A). We performed 16S ribosomal RNA (rRNA) gene sequencing of buffy coat samples and identified 65 genera belonging to four phyla (predominantly Proteobacteria) in this cohort (online supplementary figure 1 and figure 1B …

Clostridium difficile is the most important cause of nosocomial infectious diarrhea. The importance of C. difficile—associated diarrhea (CDAD) has be

Mersacidin is an antibiotic peptide produced by Bacillus sp. strain HIL Y-85,54728 that belongs to the group of lantibiotics. Its activity in vivo against methicillin-resistant Staphylococcus aureus strains compares with that of the glycopeptide antibiotic vancomycin (S. Chatterjee, D. K. Chatterjee, R. H. Jani, J. Blumbach, B. N. Ganguli, N. Klesel, M. Limbert, and G. Seibert, J. Antibiot. 45:839-845, 1992). Incubation of Staphylococcus simulans 22 with mersacidin resulted in the cessation of growth and slow lysis. Biosyntheses of DNA, RNA, and protein were not affected, whereas incorporation of glucose and D-alanine was inhibited and a regular reduction in the level of cell wall thickness was observed. Thus, unlike type A lantibiotics, mersacidin does not form pores in the cytoplasmic membrane but rather inhibits cell wall biosynthesis. Comparison with tunicamycin-treated cells indicated that peptidoglycan rather than teichoic acid metabolism is primarily affected. Mersacidin caused the excretion of a putative cell wall precursor into the culture supernatant. The formation of polymeric peptidoglycan was effectively inhibited in an in vitro assay, probably on the level of transglycosylation. In contrast to vancomycin, the activity of mersacidin was not antagonized by the tripeptide diacetyl-L-Lys-D-Ala-D-Ala, indicating that on the molecular level its mode of action differs from those of glycopeptide antibiotics. These data together with electron microscopy suggest that mersacidin acts on a novel target, which opens new perspectives for the treatment of methicillin-resistant S. aureus.

The advent of ventriculoperitoneal shunts (VPS) represented a substantial progress in the neurosurgical management of hydrocephalus in children. VPS infection is the most frequently observed complication. VPS infection is related to substantial morbidity and mortality, and exerts a negative impact on the quality of life of patients. Considerable personnel and financial resources have been devoted to its diagnosis and treatment. This article reviews the current literature and includes suggestions for the prevention, diagnosis and management of VPS infections.