Testing effectiveness of the revised Cape Town modified early warning and SBAR systems: a pilot pragmatic parallel group randomised controlled trial

Abstract Background Nurses’ recognition of clinical deterioration is crucial for patient survival. Evidence for the effectiveness of modified early warning scores (MEWS) is derived from large observation studies in developed countries. Methods We tested the effectiveness of the paper-based Cape Town (CT) MEWS vital signs observation chart and situation-background-assessment-recommendation (SBAR) communication guide. Outcomes were: proportion of appropriate responses to deterioration, differences in recording of clinical parameters and serious adverse events (SAEs) in intervention and control trial arms. Public teaching hospitals for adult patients in Cape Town were randomised to implementation of the CT MEWS/SBAR guide or usual care (observation chart without track-and-trigger information) for 31 days on general medical and surgical wards. Nurses in intervention wards received training, as they had no prior knowledge of early warning systems. Identification and reporting of patient deterioration in intervention and control wards were compared. In the intervention arm, 24 day-shift and 23 night-shift nurses received training. Clinical records were reviewed retrospectively at trial end. Only records of patients who had given signed consent were reviewed. Results We recruited two of six CT general hospitals. We consented 363 patients and analysed 292 (80.4%) patient records (n = 150, 51.4% intervention, n = 142, 48.6% control arm). Assistance was summoned for fewer patients with abnormal vital signs in the intervention arm (2/45, 4.4% versus (vs) 11/81, 13.6%, OR 0.29 (0.06–1.39)), particularly low systolic blood pressure. There was a significant difference in recording between trial arms for parameters listed on the MEWS chart but omitted from the standard observations chart: oxygen saturation, level of consciousness, pallor/cyanosis, pain, sweating, wound oozing, pedal pulses, glucose concentration, haemoglobin concentration, and “looks unwell”. SBAR was used twice. There was no statistically significant difference in SAEs (5/150, 3.3% vs 3/143, 2.1% P = 0.72, OR 1.61 (0.38–6.86)). Conclusions The revised CT MEWS observations chart improved recording of certain parameters, but did not improve nurses’ ability to identify early signs of clinical deterioration and to summon assistance. Recruitment of only two hospitals and exclusion of patients too ill to consent limits generalisation of results. Further work is needed on educational preparation for the CT MEWS/SBAR and its impact on nurses’ reporting behaviour. Trial registration Pan African Clinical Trials Registry, PACTR201406000838118. Registered on 2 June 2014, www.pactr.org

Use of Zebrafish to Probe the Divergent Virulence Potentials and Toxin Requirements of Extraintestinal Pathogenic Escherichia coli

Extraintestinal pathogenic E. coli (ExPEC) cause an array of diseases, including sepsis, neonatal meningitis, and urinary tract infections. Many putative virulence factors that might modulate ExPEC pathogenesis have been identified through sequencing efforts, epidemiology, and gene expression profiling, but few of these genes have been assigned clearly defined functional roles during infection. Using zebrafish embryos as surrogate hosts, we have developed a model system with the ability to resolve diverse virulence phenotypes and niche-specific restrictions among closely related ExPEC isolates during either localized or systemic infections. In side-by-side comparisons of prototypic ExPEC isolates, we observed an unexpectedly high degree of phenotypic diversity that is not readily apparent using more traditional animal hosts. In particular, the capacity of different ExPEC isolates to persist and multiply within the zebrafish host and cause disease was shown to be variably dependent upon two secreted toxins, α-hemolysin and cytotoxic necrotizing factor. Both of these toxins appear to function primarily in the neutralization of phagocytes, which are recruited in high numbers to sites of infection where they act as an essential host defense against ExPEC as well as less virulent E. coli strains. These results establish zebrafish as a valuable tool for the elucidation and functional analysis of both ExPEC virulence factors and host defense mechanisms

Genetics of Obesity

Obesity is caused by an imbalance between energy intake and output, influenced by numerous environmental, biological, and genetic factors. Only a minority of people with obesity have a genetic defect that is the main cause of their obesity. A key symptom for most of these disorders is early-onset obesity and hyperphagia. For some genetic obesity disorders, the hyperphagia is the main characteristic, often caused by disruptions of the leptin-melanocortin pathway, the central pathway that regulates the body's satiety and energy balance. For other disorders, obesity is part of a distinct combination of other clinical features such as intellectual disability, dysmorphic facial features, or organ abnormalities. This chapter focuses on genetic obesity disorders and also summarizes the present knowledge on the genetics of the more common polygenic/multifactorial obesity