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Roy M. Robins-Browne, The Relentless Evolution of Pathogenic Escherichia coli, Clinical Infectious Diseases, Volume 41, Issue 6, 15 September 2005, Pages 793–794, https://doi.org/10.1086/432725
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Shiga toxin (Stx)—producing strains of Escherichia coli (STEC) are important emerging pathogens. Unknown before the late 1970s, these bacteria are now recognized as a leading cause of sporadic cases and outbreaks of afebrile bloody diarrhea (“hemorrhagic colitis”) in industrialized countries and are the major cause of diarrhea-associated hemolytic uremic syndrome (HUS) worldwide [1]. STEC strains that are associated with these serious conditions are often referred to as enterohemorrhagic E. coli (EHEC) [2]. Although EHEC strains that cause HUS generally carry a number of virulence-associated determinants, the sine qua non of these bacteria is the ability to produce Stx. This toxin (also known as verotoxin, verocytotoxin, and Shiga-like toxin) occurs in 2 antigenic forms, Stx1 and Stx2, each of which has a number of allelic variants [3]. Stx1 and Stx2 are encoded by genes carried by 2 distinct λ-like bacteriophages that are integrated into the chromosome of their E. coli hosts [4]. The mechanisms of action of Stx1 and Stx2 are identical to each other and similar to that of ricin [3]. This mechanism of action involves inhibition of protein synthesis in susceptible cells, which, in the case of Stx, are predominantly endothelial cells lining small blood vessels. The damage these toxins inflict on these cells triggers intravascular coagulation, which leads to the major manifestations of HUS—namely, thrombocytopenia, microangiopathic hemolytic anemia with RBC fragmentation, and uremia, which is aggravated by the direct action of Stx on renal glomerular and tubule cells [2].
