New aspects in the pathogenesis of enteropathic hemolytic uremic syndrome

Shiga toxin (Stx) subtyping suggests that the clinical outcome of infections caused by Shiga toxin-producing Escberichia coli (STEC) depends, in large part, on the stx genotype of the infecting strain. Whereas the presence of the stx(2) or stx(2), genotype is associated with the ability of STEC to cause the hemolytic uremic syndrome (HUS), strains possessing stx(2d) or stx(2e) have been isolated from patients with less severe disease. In addition to the type of Stx, the level of Stx production might be critical for the pathogenicity of STEC. Control of Stx expression appears to be at the level of transcription. Injury to microvascular endothelial cells is the key event underlying the pathogenesis of HUS. We could show that in addition to Stx, STEC also produces other putative virulence factors, such as cytolethal distending toxin, which can contribute to the endothelial injury by interference with the cell cycle, which results in inhibition of cell proliferation and finally cell death.