Oral antibiotics in skin and soft tissue infections: An algorithm-based prospective multicentre pilot trial

Background: Skin and soft tissue infections (SSTIs) are among the most common outpatient-acquired bacterial infections. In hospitalized patients, these infections are typically treated with intravenous antibiotics, which are switched to oral formulations during the course of treatment. The optimal time point for switching from intravenous to oral treatment is unknown and depends on numerous factors. In this study, we investigated an algorithm-based switch from intravenous to oral antibiotics within 48 hours after treatment initiation. Methods: Hospitalized patients with uncomplicated SSTIs were screened for eligibility at 3 study sites (Langnau, Burgdorf, Biel/Bienne) from July 2019 to September 2020. Eligible participants with SSTIs were older than 18 years, required hospitalization because of the severity of the disease, were able to understand the study information and provided written informed consent. Exclusion criteria included antibiotic treatment 14 days or less before study inclusion, surgical site infections, impetigo without erysipelas/cellulitis, mastitis, nonbacterial infection or sterile skin inflammation (e.g., sweet syndrome, hypersensitivity reaction) and criteria consistent with “complicated” SSTIs (i.e., bacteraemia with Staphylococcus aureus or Pseudomonas aeruginosa, necrotizing fasciitis, skin abscess, septic shock or infection requiring intensive medical care, septic arthritis, osteomyelitis, tenosynovitis, bursitis, foreign body infection). Patients with a diabetic foot infection, classed on perfusion, extent, depth, infection and sensation (PEDIS) classification 3, were excluded. Other exclusion criteria included gram-negative bacteria as the causative organism for the SSTI or an ecthyma gangrenosum. After 48 hours of intravenous antibiotics, patients were assigned to either the intervention group or the non-intervention group. In the intervention group, intravenous antibiotics were switched to oral formulations. The switch was performed after 1 or more of the following predefined criteria were fulfilled: decreased pain, normalization of PEDIS grade 4 criteria, decreased or steady inflammation parameters, decreased localization and a temperature of ≤37.8°C for at least 24 hours. Patients in the non-intervention group were treated according the decision of the responsible physician. A total treatment duration of 5 to 10 days at the discretion of the treating physician was recommended. Follow-up phone calls were median conducted on day 39. Results: Of 128 screened patients, 90 were included (73 in the intervention group and 17 in the non-intervention group). Patients had a median age of 63 years, 64% were male, the majority had at least 1 comorbidity and the most affected site was the lower extremity (76.67%). In 7.8% of patients (7 cases) a microorganism was identified in blood cultures or swabs from skin blisters (5 in the intervention group and 2 in the non-intervention group). The most common isolated microorganism was group C or group G Streptococcus. The median antibiotic treatment duration was 11 days in the intervention group and 15 days in the non-intervention group; the median intravenous treatment duration was 2 days in the intervention group and 4 days in the non-intervention group; and the median duration of hospitalization was 5 days in the intervention group and 7 days in the non-intervention group. Treatment failures were noted in 3 (4%) cases in the intervention group and in 1 case (6%) in the non-intervention group. Conclusions: In this prospective pilot trial on uncomplicated SSTIs in hospitalized patients, an algorithm-based switch from intravenous to oral antibiotic treatment after a maximum of 48 hours was successful in 96% of cases. A prospective non-inferiority multicentre trial is required to confirm these results on level 1 evidence

Liquid meal composition, postprandial satiety hormones, and perceived appetite and satiety in obese women during acute caloric restriction

OBJECTIVE: The purpose of this study was to compare postprandial satiety regulating hormone responses (pancreatic polypeptide (PP) and peptide tyrosine tyrosine (PYY)) and visual analog scale- (VAS) assessed perceived appetite and satiety between liquid high-protein (HP) and high-carbohydrate (HC) meals in obese women during acute (24-h) caloric restriction. DESIGN: Eleven obese premenopausal women completed two conditions in random order in which they consumed 1500 calories as six 250-calorie HP meals or six 250-calorie HC meals over a 12-h period. Blood samples were taken at baseline and every 20 min thereafter and analyzed for PP and PYY concentrations. At these same points, perceived hunger and fullness were assessed with a VAS. The incremental area under the curve (iAUC) was used to compare postprandial responses. RESULTS: THE 12-H PP AND PYY IAUC WERE GREATER (P0.05) DURING THE HP CONDITION (PP: 4727±1306 pg/ml×12 h, PYY: 1373±357 pg/ml×12 h) compared with the HC condition (PP: 2300±528 pg/ml×12 h, PYY: 754±246 pg/ml×12 h). Perceived hunger and fullness were not different between conditions (P>0.05). The greatest changes in PYY and perceived fullness occurred after the morning meals during both conditions. CONCLUSIONS: These data suggest that in obese women during acute caloric restriction before weight loss, i) liquid HP meals, compared with HC meals, result in greater postprandial PP and PYY concentrations, an effect not associated with differential appetite or satiety responses, and ii) meal-induced changes in PYY and satiety are greatest during the morning period, regardless of dietary macronutrient composition

A New System for Automatic Radiotracking of Small Mammals

We developed a radiotracking system for automatic and continuous data collection, which allows the radiotracking of several animals at the same time. Based on a system controller, 3 fixed antennas, and small-size radiotransmitters (<2 g, 14 by 12 by 4 mm), the system has the capacity to record several individuals continuously at intervals of <5 min. Antennas, positioned at fixed points in the field, forward the signals from tagged animals to the system controller, where data are collected. The coordinates of the individual's locations are calculated through triangulation on the basis of the angles of incidence from the transmitter signal to each antenna. Transmitters are individually identified by the chronological sequence of their signals. Field tests with Microtus arvalis show the utility of the new technique and possibilities for the syste

Role of TNF-α in vascular dysfunction

Healthy vascular function is primarily regulated by several factors including EDRF (endothelium-dependent relaxing factor), EDCF (endothelium-dependent contracting factor) and EDHF (endothelium-dependent hyperpolarizing factor). Vascular dysfunction or injury induced by aging, smoking, inflammation, trauma, hyperlipidaemia and hyperglycaemia are among a myriad of risk factors that may contribute to the pathogenesis of many cardiovascular diseases, such as hypertension, diabetes and atherosclerosis. However, the exact mechanisms underlying the impaired vascular activity remain unresolved and there is no current scientific consensus. Accumulating evidence suggests that the inflammatory cytokine TNF (tumour necrosis factor)-α plays a pivotal role in the disruption of macrovascular and microvascular circulation both in vivo and in vitro. AGEs (advanced glycation end-products)/RAGE (receptor for AGEs), LOX-1 [lectin-like oxidized low-density lipoprotein receptor-1) and NF-κB (nuclear factor κB) signalling play key roles in TNF-α expression through an increase in circulating and/or local vascular TNF-α production. The increase in TNF-α expression induces the production of ROS (reactive oxygen species), resulting in endothelial dysfunction in many pathophysiological conditions. Lipid metabolism, dietary supplements and physical activity affect TNF-α expression. The interaction between TNF-α and stem cells is also important in terms of vascular repair or regeneration. Careful scrutiny of these factors may help elucidate the mechanisms that induce vascular dysfunction. The focus of the present review is to summarize recent evidence showing the role of TNF-α in vascular dysfunction in cardiovascular disease. We believe these findings may prompt new directions for targeting inflammation in future therapies