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Shiga toxins belonging to a family of structurally and functionally related protein toxins serve as the key virulence factors for pathogenecity of the virulent enteric bacterial strains namely Shigella dysenteriae serotype 1 including Shiga toxin-producing Escherichia coli (STEC). S. dysenteriae type 1 isolates remain major public health concerns due to their widespread outbreaks and the severity of extra-intestinal diseases, including acute renal failure and also affects the central nervous system. Despite practicing improved hygienic conditions and regulating food and drinking water safety, the enteric pathogens are imposing a major threat in the well being of the human society. Shiga toxin on entry into host cells’ endoplasmic reticulum (ER) activates the stress response in ER and inhibits protein synthesis by catalytic inactivation of eukaryotic ribosomes. In many cell types shiga toxins trigger apoptosis. Recent studies have shown that shiga toxins induce autophagy which activates different signaling pathways in toxin-sensitive and toxin-resistant human cells. In this review the molecular basis of Shiga toxins’ effect on host cell leading to manifestation of the infection in affected individuals are discussed with an emphasis on recent findings.
This study intended to acquire the data on Escherichia coli O157:H7 isolated from dairy cattle, heifers, and calves, and of Stx2 expressed in STEC in Chongqing. Three hundred cattle rectal faecal samples were collected and E. coli O157:H7 was identified by the isolation of the bacteria, serological tests, and PCR. Moreover, the stx2 gene's genome was examined. Three hundred and twenty six milk samples were tested for the presence of immunoglobulin G antibodies to Stx2. Six E. coli O157:H7 isolates, which did not carry stx2 were obtained from the faecal samples. Forty seven positive Stx2 antibody samples were obtained in the milk samples, whereas the Stx2 antibody was not detected in the farm where the E. coli O157:H7 isolates were obtained. The prevalence of O157:H7 is lower than the prevalence of the Stx2 antibody, and the isolates lack stx2. However, it is possible that the non-O157 STEC transfers the stx2 gene to O157:H7 horizontally, and makes O157:H7 become more virulent.
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