RESUMO
E. coli is an intestinal commensal of vertebrates. The ability to produce Shiga toxins (Stx) is the major virulence feature of Shiga toxin-producing E. coli (STEC). These potent cytotoxins block the protein synthesis by inactivating ribosomes. Their action on the target cells is responsible for the most severe forms of STEC-induced disease, such as hemorrhagic colitis and the life-threatening hemolytic uremic syndrome (HUS). Enteropathogenic E. coli (EPEC) also continues to be an important cause of infantile diarrhea in developing countries. Bundle-forming pili (bfp) are essential for the full virulence of enteropathogenic E. coli (EPEC). Exchange of genetic material between different types of bacteria, as well as with other members of the family Enterobacteriaceae in the intestinal ecosystem, leads to the appearance of normal variants of E. coli with phenetic features of pathogenicity that can serve as a theoretical basis for attributing these strains to pathobionts. PCR was used to examine 68 strains of E. coli (E. coli with normal enzymatic activity) for the presence of genes encoding the synthesis of Shiga toxins (stxl and stx2) and genes encoding the bundle-forming pilus (bfp). They were isolated from children with functional disorders of the gastrointestinal tract. The presence of the desired amplicon specific for stxl and bfp genes has resulted in formation of E. coli strains with more intense pathogenicity.
