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• W2170692443 abstract "Featherstone's (March 29, p 930)1Featherston C Escherichia coli O157: superbug or more sensation?.Lancet. 1997; 349: 930Summary Full Text Full Text PDF PubMed Google Scholar feature on Escherichia coli O157:H7 ascribes the colonic damage to the Shiga-like toxins produced by these organisms. Patients infected with enterohaemorrhagic E coli usually present with gastroenteritis, though some patients develop a dysenteric illness and occasionally systemic features, such as haemolytic-uraemic syndrome and thrombotic thrombocytopenic purpura. But factors other than the Shiga-like toxins may be involved in the development of colitis. Piglets and rabbits infected with non-toxin producing strains of O157:H7 develop diarrhoea and severe intestinal inflammation.2Tzipori S Wachsmuth KI Jackson C Studies in gnotobiotic piglets on non O157:H7 Escherichia coli serotypes isolated from patients with hemorrhagic colitis.Gastroenterology. 1988; 94: 590-597PubMed Google Scholar, 3Li Z Bell C Buret A Robins-Browne R Stiel D O'Loughlin EV The effect of enterohemorrhagic Escherichia coli O157:H7 on intestinal structure and solute transport in rabbits.Gastroenterology. 1993; 104: 467-474PubMed Google Scholar Inhibition of intestinal inflammation with an antibody directed at CD11/CD18, the β2 integrin on polymorphonuclear phagocytes, prevents the mucosal injury in rabbits infected with O157:H7.4Elliot E Li Z Bell C et al.Modulation of host response to Escherichia coli O157:H7 infection by anti-CD18 antibody in rabbits.Gastroenterology. 1994; 106: 1554-1561PubMed Google Scholar These findings indicate an important role for host-defence mechanisms in the intestinal injury.Shiga-like toxins bind to endothelial cells, particularly in blood vessels in the intestinal microcirculation, kidney, and brain. Sjogren and colleagues5Sjogren R Neill R Rachmilewitz D et al.Role of Shiga-like toxin 1 in bacterial enteritis: comparison between isogenic Escherichia coli strains induced in rabbits.Gastroenterology. 1994; 106: 306-317PubMed Google Scholar study of rabbit diarrhoeagenic E coli (RDEC) expressing Shiga-like toxins 1, indicate that the toxin causes microvascular thrombosis in the mucosal circulation at a late stage in the course of the disease, which exacerbates the injury usually associated with isogenic nontoxin producing strains. This thrombosis results in a severe dysenteric illness which does not occur in wild RDEC. Thus, a slightly different model of disease pathogenesis emerges. Enterohaemorrhagic E coli infect the large intestine and induce a inflammatory response in the host. The resultant injury allows luminal Shiga-like toxins, produced by the bacteria, to enter the circulation where they bind to endothelial receptors on mucosal vessels. The toxin induces microvascular thrombosis and an ischaemic injury in the intestine which worsen diarrhoea and leads to dysentery. There is only limited experimental data to indicate that the toxins themselves injure the epithelial cells. Distant organ damage in brain, kidney, pancreas, or skin occurs if enough toxins enter the systemic circulation and bind to endothelial receptors in distant sites. This model of pathogenesis has important implications for disease prevention. Systemic vaccination against Shiga-like toxins is likely to prevent the severe systemic signs of the disease, such as haemolytic-uraemic syndrome, and ameliorate the severe dysentery. However, such vaccination is unlikely to prevent gastroenteritis in infected individuals. Featherstone's (March 29, p 930)1Featherston C Escherichia coli O157: superbug or more sensation?.Lancet. 1997; 349: 930Summary Full Text Full Text PDF PubMed Google Scholar feature on Escherichia coli O157:H7 ascribes the colonic damage to the Shiga-like toxins produced by these organisms. Patients infected with enterohaemorrhagic E coli usually present with gastroenteritis, though some patients develop a dysenteric illness and occasionally systemic features, such as haemolytic-uraemic syndrome and thrombotic thrombocytopenic purpura. But factors other than the Shiga-like toxins may be involved in the development of colitis. Piglets and rabbits infected with non-toxin producing strains of O157:H7 develop diarrhoea and severe intestinal inflammation.2Tzipori S Wachsmuth KI Jackson C Studies in gnotobiotic piglets on non O157:H7 Escherichia coli serotypes isolated from patients with hemorrhagic colitis.Gastroenterology. 1988; 94: 590-597PubMed Google Scholar, 3Li Z Bell C Buret A Robins-Browne R Stiel D O'Loughlin EV The effect of enterohemorrhagic Escherichia coli O157:H7 on intestinal structure and solute transport in rabbits.Gastroenterology. 1993; 104: 467-474PubMed Google Scholar Inhibition of intestinal inflammation with an antibody directed at CD11/CD18, the β2 integrin on polymorphonuclear phagocytes, prevents the mucosal injury in rabbits infected with O157:H7.4Elliot E Li Z Bell C et al.Modulation of host response to Escherichia coli O157:H7 infection by anti-CD18 antibody in rabbits.Gastroenterology. 1994; 106: 1554-1561PubMed Google Scholar These findings indicate an important role for host-defence mechanisms in the intestinal injury. Shiga-like toxins bind to endothelial cells, particularly in blood vessels in the intestinal microcirculation, kidney, and brain. Sjogren and colleagues5Sjogren R Neill R Rachmilewitz D et al.Role of Shiga-like toxin 1 in bacterial enteritis: comparison between isogenic Escherichia coli strains induced in rabbits.Gastroenterology. 1994; 106: 306-317PubMed Google Scholar study of rabbit diarrhoeagenic E coli (RDEC) expressing Shiga-like toxins 1, indicate that the toxin causes microvascular thrombosis in the mucosal circulation at a late stage in the course of the disease, which exacerbates the injury usually associated with isogenic nontoxin producing strains. This thrombosis results in a severe dysenteric illness which does not occur in wild RDEC. Thus, a slightly different model of disease pathogenesis emerges. Enterohaemorrhagic E coli infect the large intestine and induce a inflammatory response in the host. The resultant injury allows luminal Shiga-like toxins, produced by the bacteria, to enter the circulation where they bind to endothelial receptors on mucosal vessels. The toxin induces microvascular thrombosis and an ischaemic injury in the intestine which worsen diarrhoea and leads to dysentery. There is only limited experimental data to indicate that the toxins themselves injure the epithelial cells. Distant organ damage in brain, kidney, pancreas, or skin occurs if enough toxins enter the systemic circulation and bind to endothelial receptors in distant sites. This model of pathogenesis has important implications for disease prevention. Systemic vaccination against Shiga-like toxins is likely to prevent the severe systemic signs of the disease, such as haemolytic-uraemic syndrome, and ameliorate the severe dysentery. However, such vaccination is unlikely to prevent gastroenteritis in infected individuals." @default.
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• W2170692443 title "Escherichia coli O157:H7" @default.
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