Shiga toxin (Stx)-producing Escherichia coli (STEC) is an etiologic agent of bloody
diarrhea. A serious sequela of disease, the
hemolytic uremic syndrome (HUS) may arise in up to 25% of patients. The development of HUS after STEC
infection is linked to the presence of Stx. STEC strains may produce one or more Stxs, and the Stxs come in two major immunological groups, Stx1 and Stx2. A multitude of possible
therapeutics designed to inhibit the actions of the Stxs have been developed over the past 30 years. Such
therapeutics are important because
antibiotic treatment of STEC
infections is contraindicated due to an increased potential for development of HUS. The reason for the increased risk of HUS after
antibiotic treatment is likely because certain
antibiotics induce expression of the Stxs, which are generally associated with lysogenic bacteriophages. There are a few potential
therapeutics that either try to kill STEC without inducing Stx expression or target gene expression within STEC. However, the vast majority of the treatments under development are designed to limit Stx receptor generation or to prevent toxin binding, trafficking, processing, or activity within the cell. The potential
therapies described in this review include some that have only been tested in vitro and several that demonstrate efficacy in animals. The
therapeutics that are currently the furthest along in development (completed phase I and II trials) are
monoclonal antibodies directed against Stx1 and Stx2.