scholarly journals Correction to: Characteristics and prognosis of bloodstream infection in patients with COVID‑19 admitted in the ICU: an ancillary study of the COVID‑ICU study

2022 ◽  
Vol 12 (1) ◽  
Author(s):  
Nicolas Massart ◽  
Virginie Maxime ◽  
Pierre Fillatre ◽  
Keyvan Razazi ◽  
Alexis Ferré ◽  
...  
2019 ◽  
Vol 14 (1) ◽  
pp. 47-49
Author(s):  
Basant K. Puri ◽  
Anne Derham ◽  
Jean A. Monro

Background: The use of indwelling Central Venous Access Devices (CVADs) is associated with the development of bloodstream infections. When CVADs are used to administer systemic antibiotics, particularly second- or higher-generation cephalosporins, there is a particular risk of developing Clostridium difficile infection. The overall bloodstream infection rate is estimated to be around 1.74 per 1000 Central Venous Catheter (CVC)-days. Objective: We hypothesised that daily oral administration of the anion-binding resin colestyramine (cholestyramine) would help prevent infections in those receiving intravenous antibiotic treatment via CVADs. Method: A small case series is described of adult patients who received regular intravenous antibiotic treatment (ceftriaxone, daptomycin or vancomycin) for up to 40 weeks via indwelling CVADs; this represented a total of 357 CVC-days. In addition to following well-established strategies to prevent C. difficile infection, during the course of the intravenous antibiotic treatment the patients also received daily oral supplementation with 4 g colestyramine. Results: There were no untoward infectious events. In particular, none of the patients developed any symptoms or signs of C. difficile infection, whereas approximately one case of a bloodstream infection would have been expected. Conclusion: It is suggested that oral colestyramine supplementation may help prevent such infection through its ability to bind C. difficile toxin A (TcdA) and C. difficile toxin B (TcdB); these toxins are able to gain entry into host cells through receptor-mediated endocytosis, while anti-toxin antibody responses to TcdA and TcdB have been shown to induce protection against C. difficile infection sequelae.


2020 ◽  
Vol 88 (8) ◽  
Author(s):  
Danelle R. Weakland ◽  
Sara N. Smith ◽  
Bailey Bell ◽  
Ashootosh Tripathi ◽  
Harry L. T. Mobley

ABSTRACT Serratia marcescens is a bacterium frequently found in the environment, but over the last several decades it has evolved into a concerning clinical pathogen, causing fatal bacteremia. To establish such infections, pathogens require specific nutrients; one very limited but essential nutrient is iron. We sought to characterize the iron acquisition systems in S. marcescens isolate UMH9, which was recovered from a clinical bloodstream infection. Using RNA sequencing (RNA-seq), we identified two predicted siderophore gene clusters (cbs and sch) that were regulated by iron. Mutants were constructed to delete each iron acquisition locus individually and in conjunction, generating both single and double mutants for the putative siderophore systems. Mutants lacking the sch gene cluster lost their iron-chelating ability as quantified by the chrome azurol S (CAS) assay, whereas the cbs mutant retained wild-type activity. Mass spectrometry-based analysis identified the chelating siderophore to be serratiochelin, a siderophore previously identified in Serratia plymuthica. Serratiochelin-producing mutants also displayed a decreased growth rate under iron-limited conditions created by dipyridyl added to LB medium. Additionally, mutants lacking serratiochelin were significantly outcompeted during cochallenge with wild-type UMH9 in the kidneys and spleen after inoculation via the tail vein in a bacteremia mouse model. This result was further confirmed by an independent challenge, suggesting that serratiochelin is required for full S. marcescens pathogenesis in the bloodstream. Nine other clinical isolates have at least 90% protein identity to the UMH9 serratiochelin system; therefore, our results are broadly applicable to emerging clinical isolates of S. marcescens causing bacteremia.


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