Pathogenesis and treatment of Shiga toxin-producing Escherichia coli infections

Abstract

Improved understanding of Shiga toxin-producing Escherichia coli pathophysiology and progression to hemolytic uremic syndrome provides the basis for prevention, prophylactic and treatment strategies.

Identification and characterization of Cri1, a locus controlling mortality during Citrobacter rodentium infection in mice

“…(c) Examination of the frequency distribution of the survival in the (C3  B6)F2 mice reveals that the phenotype is not normally distributed and presents a major spike in the distribution at day 30 (censored data, shown with crosshatched pattern). Also, when considering only nonsurviving mice (noncensored data), the phenotype is not normally distributed as there is a sharp increase in mortality early in infection (days [10][11][12][13][14] and then a gradual decrease in mortality up to days 24-27, leading to a distribution with a long 'tail' toward the right-hand side of the graph. (d) Examination of the frequency distribution of the survival in the (C3Ou  B6)F2 mice reveals an even larger spike in the distribution at day 30 (censored data).…”

“…The survival time distribution for C3OuB6F2 mice reveals an even larger spike of surviving mice at day 30 ( Figure 2d). When considering only nonsurviving mice (noncensored data), the phenotype is not normally distributed either: there is a sharp increase in mortality early in infection (days [10][11][12][13][14] and then a gradual decrease in mortality up to days 24-27, leading to a distribution with a long 'tail' toward the right-hand side of the graph. This is seen in both crosses, although it is more evident in the C3 cross (Figures 2c and d).…”

“…10 These observations are all the more worrisome as there are currently no specific therapeutic regimens for EHEC infections; antibiotic use is not recommended as it exacerbates disease and increases the rate of development of complications. 11 The parallels between C. rodentium infection of mice and EHEC and EPEC infection of humans are striking. These Enterobacteriaceae colonize the gastrointestinal tract of their hosts by the formation of characteristic attaching/effacing lesions, leading to the development of diarrhea, colitis and hyperplasia of the intestinal epithelium.…”

Probiotics prevent enterohaemorrhagic Escherichia coli O157 : H7-mediated inhibition of interferon-γ-induced tyrosine phosphorylation of STAT-1

“…This foodborne enteric pathogen is acquired from contaminated foodstuffs and non-chlorinated drinking water (Karch et al, 2005;Maki, 2006;Rangel et al, 2005). In the severest cases of infection (~10-15 % of cases), the haemolytic uraemic syndrome develops as a systemic complication, leading to patient hospitalization, kidney failure and death (Serna & Boedeker, 2008;Tarr et al, 2005). Renal disease results from bacterial cytotoxin [Shiga-like toxin (Stx)-1 and -2] production in the gut, release into the systemic circulation and damage to vascular endothelial cells in the renal glomerulus (Blackall & Marques, 2004).…”

“…Outbreaks of enterohaemorrhagic Escherichia coli (EHEC) serotype O157 : H7 infection occur frequently across the developed world (Serna & Boedeker, 2008). This foodborne enteric pathogen is acquired from contaminated foodstuffs and non-chlorinated drinking water (Karch et al, 2005;Maki, 2006;Rangel et al, 2005).…”