ABSTRACT
GI endoscopy is highly resource-intensive with a significant contribution to greenhouse gas (GHG) emissions and waste generation. Sustainable endoscopy in the context of climate change is now the focus of mainstream discussions between endoscopy providers, units and professional societies. In addition to broader global challenges, there are some specific measures relevant to endoscopy units and their practices, which could significantly reduce environmental impact. Awareness of these issues and guidance on practical interventions to mitigate the carbon footprint of GI endoscopy are lacking. In this consensus, we discuss practical measures to reduce the impact of endoscopy on the environment applicable to endoscopy units and practitioners. Adoption of these measures will facilitate and promote new practices and the evolution of a more sustainable specialty.
Subject(s)
Gastroenterology , Humans , Consensus , Endoscopy, GastrointestinalABSTRACT
Enterohaemorrhagic Escherichia coli (EHEC) is a major foodborne pathogen and tightly adheres to human colonic epithelium by forming attaching/effacing lesions. To reach the epithelial surface, EHEC must penetrate the thick mucus layer protecting the colonic epithelium. In this study, we investigated how EHEC interacts with the intestinal mucus layer using mucin-producing LS174T colon carcinoma cells and human colonic mucosal biopsies. The level of EHEC binding and attaching/effacing lesion formation in LS174T cells was higher compared to mucin-deficient colon carcinoma cell lines, and initial adherence was independent of the presence of flagellin, Escherichia coli common pilus, or long polar fimbriae. Although EHEC infection did not affect gene expression of secreted mucins, it resulted in reduced MUC2 glycoprotein levels. This effect was dependent on the catalytic activity of the secreted metalloprotease StcE, which reduced the inner mucus layer and thereby promoted EHEC access and binding to the epithelium in vitro and ex vivo. Given the lack of efficient therapies against EHEC infection, StcE may represent a suitable target for future treatment and prevention strategies.
Subject(s)
Bacterial Adhesion/physiology , Escherichia coli Infections/pathology , Escherichia coli O157/pathogenicity , Escherichia coli Proteins/metabolism , Intestinal Mucosa/microbiology , Metalloendopeptidases/metabolism , Mucus/metabolism , Bacterial Adhesion/genetics , Caco-2 Cells , Cell Line , Colon/microbiology , Colon/pathology , Escherichia coli Infections/microbiology , Escherichia coli O157/genetics , Escherichia coli O157/metabolism , Escherichia coli Proteins/genetics , Fimbriae, Bacterial/metabolism , Flagellin/metabolism , HT29 Cells , Humans , Intestinal Mucosa/pathology , Metalloendopeptidases/genetics , Mucin-2/metabolismABSTRACT
Enteroaggregative E. coli (EAEC) are a major cause of diarrhoea worldwide. Due to their heterogeneity and carriage in healthy individuals, identification of diagnostic virulence markers for pathogenic strains has been difficult. In this study, we have determined phenotypic and genotypic differences between EAEC strains of sequence types (STs) epidemiologically associated with asymptomatic carriage (ST31) and diarrhoeal disease (ST40). ST40 strains demonstrated significantly enhanced intestinal adherence, biofilm formation, and pro-inflammatory interleukin-8 secretion compared with ST31 isolates. This was independent of whether strains were derived from diarrhoea patients or healthy controls. Whole genome sequencing revealed differences in putative virulence genes encoding aggregative adherence fimbriae, E. coli common pilus, flagellin and EAEC heat-stable enterotoxin 1. Our results indicate that ST40 strains have a higher intrinsic potential of human pathogenesis due to a specific combination of virulence-related factors which promote host cell colonization and inflammation. These findings may contribute to the development of genotypic and/or phenotypic markers for EAEC strains of high virulence.
Subject(s)
Biofilms/growth & development , Escherichia coli Infections , Escherichia coli Proteins , Escherichia coli , Virulence Factors , Escherichia coli/pathogenicity , Escherichia coli/physiology , Escherichia coli Infections/genetics , Escherichia coli Infections/metabolism , Escherichia coli Proteins/genetics , Escherichia coli Proteins/metabolism , HeLa Cells , Humans , Virulence Factors/genetics , Virulence Factors/metabolismABSTRACT
CONTEXT: Acute pancreatitis due to pancreatic ischemia is a rare condition. CASE REPORT: In this case report we describe a 57-year-old male who developed an acute necrotizing pancreatitis after running a marathon and visiting a sauna the same evening, with an inadequate fluid and food consumption during both events. CONCLUSIONS: Pancreatic ischemia imposed by mechanical and physical stress and dehydration can induce the development of acute pancreatitis. Separately, these factors are rare causes of ischemic acute pancreatitis. But when combined, as in this particular case, the risk of an acute necrotizing pancreatitis cannot be neglected.