Shiga Toxin-Producing Escherichia Coli

This chapter discusses the emergence and impact of shiga toxin-producing Escherichia coli (STEC) in human disease, the biology of the Shiga toxins (Stx) family, and approaches to diagnosis, treatment, and prevention of infection with STEC. The occurrence of the seminal STEC outbreaks highlighted the need to implement laboratory methods to readily detect E. coli O157:H7. Although early characterization of STEC strains was made possible by Whittam’s multilocus enzyme electrophoresis (MLEE) method, genetic techniques now allow comparison of strains at the nucleotide level. The current model of the predominant pathway by which Stx intoxicates sensitive cells is as follows: (i) the B pentamer of holotoxin binds to Gb3 within lipid rafts; (ii) the entire receptor-holotoxin complex is endocytosed; (iii) the complex moves by retrograde transport to the Golgi and then to the endoplasmic reticulum; and (iv) the A1 subunit is released into the cytoplasm, where it targets the ribosome. Although transduction of stx genes into E. coli via bacteriophages was crucial to the emergence of STEC, the biology of these toxin-converting phages also contributes significantly to the degree of toxin expression and hence the virulence exhibited by STEC. Although the pathogenicity of various STEC strains that synthesize different types of Stx2 cannot be compared directly because the strains are not isogenic, the authors have found that an O91 strain that produces Stx2 is not virulent in the streptomycin-treated mouse model for STEC infection, whereas O91 strains that produce Stx2d-activatable are highly virulent in those mice.