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Introduction: Enteric infection with Clostridioides difficile , Escherichia coli subtypes, and norovirus is commonly detected in flares of inflammatory bowel disease (IBD). We associated the gut microbiome during flare complicated by a gastrointestinal pathogen with outcomes of IBD., Methods: We performed a cross-sectional study of 260 patients (92 IBD and 168 non-IBD) with a gastrointestinal polymerase chain reaction panel positive for C. difficile, E. coli , or norovirus, or negative during an episode of diarrhea from 2018 to 2020, and 25 healthy controls. Clinical variables, IBD status, and 2-year outcomes were collected. Using 16S rRNA sequencing, we measured the effect size of the gut microbiome on IBD characteristics and outcomes., Results: There were major differences in the gut microbiome between patients with and without a pathogen and IBD. In IBD, a higher proportion of patients without a pathogen required hospitalization and IBD therapies at flare and within the 2 years after flare, driven by a milder disease course in flares complicated by an E. coli subtype or norovirus. Examining the contribution of clinical covariates, the presence of IBD, and C-reactive protein, C. difficile had a greater relative influence on the gut microbiome compared with the presence of an E. coli subtype or norovirus. In patients with C. difficile or no pathogen, lower microbiome diversity at flare was associated with adverse IBD outcomes over 2 years., Discussion: Distinctive pathogen-specific gut microbiomes were associated with subsequent IBD outcomes. These findings may have direct implications for the management of IBD flares complicated by enteric pathogens., (Copyright © 2023 The Author(s). Published by Wolters Kluwer Health, Inc. on behalf of The American College of Gastroenterology.)

Background: The initiating events of chronic gastrointestinal (GI) inflammation in Crohn's disease (CD) and ulcerative colitis (UC) are not well-defined, but GI infections are implicated., Aims: To define the role of GI infections in risk of incident inflammatory bowel disease (IBD) and synthesise the current body of relevant translational data to provide biological context for associations between GI infections and IBD risk., Methods: We systematically reviewed electronic databases through February 2020. Clinical studies that provided risk estimates of the association between GI infections and incident IBD were included. Inclusion criteria were broader for translational studies aiming to define mechanisms of GI infections and predisposition to or protection from IBD., Results: Of the studies identified, 63 met full inclusion criteria. Among studies of clinical gastroenteritis, bacteria-specifically, Salmonella species, Campylobacter species and Clostridioides difficile-demonstrated consistent positive associations with risk of incident IBD. Of viruses, norovirus was associated with increased risk of incident CD. Regarding inverse associations with incident IBD, Helicobacter pylori and helminth infections were associated with a generally consistent reduced risk of IBD. Based on a qualitative analysis of the translational data, putative mechanisms involve multiple microbial and immunologic pathways., Conclusions: Based on this systematic review, certain enteric pathogens are associated with an increased risk of incident IBD, while others are potentially protective. Prospective studies are required to clarify the clinical implications of these enteric pathogens on the risk and course of IBD, and possible therapeutic or preventative benefit., (© 2020 John Wiley & Sons Ltd.)

Background: Gastrointestinal infection is a major cause of morbidity. We sought to characterize the pathogenic etiologies of gastrointestinal infection to identify seasonal patterns and predictors of specific infections utilizing a multiplex PCR assay in clinical practice.Methods: We performed a cross-sectional study of 9403 patients who underwent 13,231 stool tests with a FilmArray gastrointestinal pathogen PCR panel during an episode of diarrhea from March 2015 to May 2017. Our primary outcome was the presence of a positive panel. Logistic regression was used to test for associations between season and infections.Results: A positive result was found in 3426 tests (25.9%) in 2988 patients (31.8%), yielding 4667 pathogens consisting of 1469 viruses (31.5%), 2925 bacteria (62.7%), and 273 parasites (5.8%). Age less than 50 years was associated with a higher prevalence of pathogens compared to age ≥ 50 (p < 0.0001). The overall prevalence of a positive result for bacteria peaked in the summer (635, 29.2%), and the prevalence of viruses peaked in the winter (446, 31.8%). Compared to the winter, testing in the summer yielded a higher prevalence of bacteria (OR 1.52, 95% CI 1.33, 1.73, p < 0.0001) and lower odds of viruses (OR 0.69, 95% CI 0.58, 0.81, p < 0.0001), primarily driven by E. coli species and norovirus.Conclusions: Season was a major determinant in detecting specific pathogens. Our substantially lower positivity rate than previous reports in the literature on multiplex PCR assays may more accurately reflect true clinical practice. Recognizing the temporal distribution of enteric pathogens may help facilitate empiric treatment decisions in certain clinical situations. [ABSTRACT FROM AUTHOR]

Background: Gut colonization with vancomycin-resistant Enterococcus (VRE) is associated with poor outcomes. This study evaluated the impact of VRE colonization on subsequent acquisition of enteric pathogens. Methods: We performed a retrospective cohort study of adults admitted to an ICU from 2012 to 2017 who were screened for VRE colonization and subsequently underwent stool testing with a gastrointestinal pathogen PCR panel (GI PCR) with or without PCR testing for Clostridium difficile. Our primary outcome was the presence of any enteric pathogen. Cox proportional hazards modeling was used to adjust for factors associated with enteric infection. Results: Of 761 patients who underwent VRE screening and subsequent GI PCR, 131 (17%) were colonized with VRE. Patients with VRE colonization were less likely to test positive on GI PCR compared to patients without VRE (9.2% vs 18%, p = 0.01); specifically for E. coli species (p = 0.03) and viral (p = 0.04) enteric infections. In 716 patients who underwent C. difficile testing, there was a trend towards more C. difficile infections in patients colonized with VRE (15% vs 10%, p = 0.11). On multivariable analysis, patients with VRE had a decreased risk of a positive GI PCR (aHR 0.47, 95% CI 0.25–0.88, p = 0.02) but not C. difficile infection, effects which persisted during 5 years of follow-up. Among positive tests, there was a greater proportion of C. difficile with VRE (57% vs 28%, p < 0.01). Conclusions: VRE colonization was associated with a decreased risk of subsequent non-C. difficile enteric infection. VRE domination of the gut microbiome may protect against acquisition of common enteric pathogens. [ABSTRACT FROM AUTHOR]