Role of bacterial toxins in pathogenesis of hemolytic-uremic syndrome, caused by enterohemorrhagic Escherichia

The pathogenesis of the hemolytico-uremic syndrome (HUS) caused by enterohemorrhagic E. coli (EHEC) has been studied previously rather completely. HUS is characterized by the signs of microangiopathic hemolytic anemia, thrombocytopenia with renal lesions and manifestations of transient disturbances in the functions of the central nervous system. The adherence of EHEC to enterocytes was found to occur in the terminal section of the ileum and the large intestine. This process is realized with involvement intimin, EHEC outer membrane protein. Shiga-like toxins (SLT) produced by EHEC are the leading factor of their pathogenicity. The mechanism of the toxin translocation through enterocytes is not yet clear, still there is no doubt that SLT penetrates into the systemic blood stream. This is indicated by the results of histopathological studies it possible to find the toxin traces on the membranes of endothelial cells of blood vessels. The study reveals that the cells of the vascular epithelium are highly sensitive to SLT. These cells carry receptors Gb3, also known as CD77, on their membranes. Enterohemolysin, serine protease, causing disturbances in the barrier function of the intestine, can be regarded in the pathogenesis of hemorrhagic colitis which develops as the result of the damaging action of EHEC and the above-mentioned toxins. This leads to the increased level of blood systemic bacterial lipopolysaccharides, which may play, in combination with the action of SLT, an important role in the development of multi-organ pathology in HUS patients.