Bacterial infection and thrombosis are highly correlated, especially in patients with indwelling medical devices. Coagulase-negative staphylococci, typified by Staphylococcus epidermidis, are a common cause of medical device infections owing to their biofilm forming capacity which provides protection from antibiotics and host immune response. Attention has been drawn to the interaction between S. epidermidis and host proteins, specifically fibrinogen. However, little is known regarding the impact of the transition from planktonic to biofilm forming phenotype on this interaction. Here we investigate the growth phase dependence of bacteria-fibrinogen interaction and the resulting effect on fibrin clot formation, structure, and mechanics. Flow cytometry demonstrated growth phase dependent affinity for fibrinogen. To mimic intravascular device seeding, we quantified the adhesion of S. epidermidis to a fibrinogen coated surface under continuous flow conditions in vitro. The bacterial deposition rate onto fibrinogen was significantly greater for stationary (5,360 ± 1,776 cells/cm2s) versus exponential phase (2,212 ± 264, cells/cm2 s). Furthermore, the expression of sdrG–a cell surface adhesion protein with specificity for fibrinogen–was upregulated ∼twofold in the stationary versus the exponential phase. Rheometry and confocal microscopy demonstrated that stationary phase S. epidermidis slows clot formation and generates a more heterogeneous fibrin network structure with greater elasticity (G′ = 5.7 ± 1.0 Pa) compared to sterile fibrinogen (G′ = l.5 ± 0.2 Pa), while exponential phase cells had little effect. This work contributes to the current understanding of the growth phase dependent regulation of bacterial virulence factors and the correlation between bacterial infection and thrombosis.
We report two cases of acute hypotension after intravenous azithromycin administration in children with acute, decompensated heart failure. In each of our reported cases, azithromycin was being used to treat possible Mycoplasma myocarditis. In this report, we aim to describe hypotension as a potentially rare adverse reaction to intravenous azithromycin and encourage judicious use in patients with cardiac dysfunction.
Bacterial infection is known to increase the risk for thromboembolism. The mechanism underlying this correlation remains largely unknown. We recently showed that the common pathogen Staphylococcus epidermidis retards clot formation, increases clot elasticity and generates a heterogeneous clot structure that remodels over time. Here, we elucidate the mechanism of this process by evaluating the capacity for S. epidermidis to bind to fibrinogen as a function of its growth phase. We hypothesized that the effect of S. epidermidis on a fibrin clot is related to its propensity toward biofilm formation. Therefore, stationary phase (biofilm-like) S. epidermidis will have a more robust effect on clot kinetics and elasticity than exponential phase (planktonic). Furthermore, this difference is mediated by increased adhesion to fibrinogen. Rheometry was used to evaluate the formation and resultant elasticity of fibrin clots with exponential or stationary phase S. epidermidis . A functional in vitro model was developed to evaluate adhesion of S. epidermidis to a fibrinogen coated surface in a continuously flowing environment. Fluorescent labeled exponential and stationary phase S. epidermidis were visualized flowing through a parallel plate microfluidic chamber past immobilized fibrinogen. Images were obtained every 3 seconds for 30 min. Bacterial deposition rate and mean adhesion time were quantified by automated image analysis. A paired Student’s t-test was used for statistical analysis. Stationary phase S. epidermidis retards clot formation and increases resultant elasticity while exponential phase only slightly reduces elasticity. The bacterial deposition rate onto fibrinogen was significantly (p=0.03) greater for stationary phase (1741 ± 1513 cells/cm 2 · sec -1 ) vs exponential phase (676 ± 270 cells/cm 2 · sec -1 ). The average adhesion time however was similar for exponential and stationary phase cells. Coagulation proteins can provide a framework for bacterial adhesion, biofilm formation and infection. In turn infected thrombi with (biofilm-like) bacteria are stiffer which correlates to more frequent bacterial binding to fibrinogen. This provides a potential molecular mechanism for infection mediated thromboembolic events.
Background: Burnout is well characterised in physicians and residents but not in paediatric cardiology fellows, and few studies follow burnout longitudinally. Training-specific fears have been described in paediatric cardiology fellows but also have not been studied at multiple time points. This study aimed to measure burnout, training-specific fears, and professional fulfilment in paediatric cardiology fellows with the attention to time of year and year-of-training. Methods: This survey-based study included the Professional Fulfillment Index and the Impact of Events Scale as well as an investigator-designed Fellow Fears Questionnaire. Surveys were distributed at three-time points during the academic year to paediatric cardiology fellows at a large Midwestern training programme. Fellow self-reported gender and year-of-training were collected. Descriptive analyses were performed. Results: 10/17 (59%) of fellows completed all surveys; 60% were female, 40% in the first-year class, 40% in the second-year class, and 20% in the third-year class. At least half of the fellows reported burnout at each survey time point, with lower mean professional fulfilment scores. The second-year class, who rotate primarily in the cardiac ICU, had higher proportions of burnout than the other two classes. At least half of fellows reported that they “often” or “always” worried about not having enough clinical knowledge or skills and about work–life balance. Conclusions: Paediatric cardiology fellows exhibit high proportions of burnout and training-specific fears. Interventions to mitigate burnout should be targeted specifically to training needs, including during high-acuity rotations.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
customersupport@researchsolutions.com
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
This site is protected by reCAPTCHA and the Google Privacy Policy and Terms of Service apply.
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.