Antimicrobial resistance (AMR) is currently one of the most important challenges to the treatment of bacterial infections. A critical issue to combat AMR is to restrict its spread. In several instances, bacterial plasmids are involved in the global spread of AMR. Plasmids belonging to the incompatibility group (Inc)HI are widespread in Enterobacteriaceae and most of them express multiple antibiotic resistance determinants. They play a relevant role in the recent spread of colistin resistance. We present in this report novel findings regarding IncHI plasmid conjugation. Conjugative transfer in liquid medium of an IncHI plasmid requires expression of a plasmid-encoded, large-molecular-mass protein that contains an Ig-like domain. The protein, termed RSP, is encoded by a gene (ORF R0009) that maps in the Tra2 region of the IncHI1 R27 plasmid. The RSP protein is exported outside the cell by using the plasmid-encoded type IV secretion system that is also used for its transmission to new cells. Expression of the protein reduces cell motility and enables plasmid conjugation. Flagella are one of the cellular targets of the RSP protein. The RSP protein is required for a high rate of plasmid transfer in both flagellated and nonflagellated Salmonella cells. This effect suggests that RSP interacts with other cellular structures as well as with flagella. These unidentified interactions must facilitate mating pair formation and, hence, facilitate IncHI plasmid conjugation. Due to its location on the outer surfaces of the bacterial cell, targeting the RSP protein could be a means of controlling IncHI plasmid conjugation in natural environments or of combatting infections caused by AMR enterobacteria that harbor IncHI plasmids.

Serratia marcescens N28b produces bacteriocin 28b, active against Escherichia coli. Bacteriocin sensitivity tests performed on a collection of E. coli envelope mutants, and isolation and characterization of E. coli bacteriocin-28b-insensitive mutants, showed that the core lipopolysaccharide, outer membrane proteins OmpA and OmpF, and TolQ, TolA, and TolB proteins are involved in bacteriocin 28b lethal activity. These mutants are assayed for bacteriocin 28b sensitivity under normal and bypass conditions, and their bacteriocin-binding ability was determined. The results obtained suggest that the core lipopolysaccaride and outer membrane proteins OmpA and OmpF are involved in bacteriocin 28b binding. Furthermore, bacteriocin 28b translocation requires proteins TolA, TolB, and TolQ.

Chronic spontaneous urticaria (CSU) is a heterogeneous condition that can severely impact quality of life, which is why rapid disease control is essential. Symptomatic first-line treatment of CSU is the licensed dose of second-generation H1 antihistamines. For second-line treatment, this dose may be increased by up to four times. In patients who fail to respond to these higher doses of H1 antihistamines, treatment with omalizumab (up to 24 weeks) is recommended to achieve disease control. After this 24-week period, the patient response profile to omalizumab should be defined in order to identify refractory patients. The optimal management approach for refractory patients has not been established. In this context, the aim of the present expert consensus study involving a group of specialists (allergists and dermatologists) with specific expertise in treating urticaria was to define specific patient profiles based on their differing responses to omalizumab. Another objective was to develop a treatment algorithm based on the specific response profile. First, a comprehensive literature review was conducted. Then, a group meeting was held to discuss all issues related to the therapeutic management of these patients that had not been addressed in any previous studies. In all cases, the experts considered both the available evidence and their own clinical experience with omalizumab. We believe that implementation of this proposed algorithm will help to optimise the management of CSU patients who are refractory to antihistamine treatment, reduce disease-related costs, and improve QoL.

BackgroundFood allergy is an abnormal immunological response following exposure (usually ingestion) to a food. Elimination of the allergen is the principle treatment for food allergy, including allergy to fruit. Accidental ingestion of allergenic foods can result in severe anaphylactic reactions. Allergen-specific immunotherapy (SIT) is a specific treatment, when the avoidance of allergenic foods is problematic. Recently, studies have been conducted on di erent types of immunotherapy for the treatment of food allergy, including oral (OIT) and sublingual immunotherapy (SLIT). ObjectivesTo determine the e icacy and safety of oral and sublingual immunotherapy in children and adults with food allergy to fruits, when compared with placebo or an elimination strategy. Search methodsThe Cochrane Central Register of Controlled Trials (CENTRAL), MEDLINE, EMBASE, CINAHL, and AMED were searched for published results along with trial registries and the Journal of Negative Results in BioMedicine for grey literature. The date of the most recent search was July 2015. Selection criteriaRandomised controlled trials (RCTs) comparing OIT or SLIT with placebo or an elimination diet were included. Participants were children or adults diagnosed with food allergy who presented immediate fruit reactions.Immunotherapy (oral and sublingual) for food allergy to fruits (Review)

Transmission of a plasmid from one bacterial cell to another, in several instances, underlies the dissemination of antimicrobial resistance (AMR) genes. The process requires well-characterized enzymatic machinery that facilitates cell-to-cell contact and the transfer of the plasmid.