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Enterohemorrhagic Escherichia coli (EHEC) serotype O157:H7 is a human pathogen responsible for outbreaks of bloody diarrhea and hemolytic uremic syndrome worldwide. Conventional antimicrobials trigger an SOS response in EHEC that promotes the release of the potent Shiga toxin that is responsible for much of the morbidity and mortality associated with EHEC infection. Cattle are a natural reservoir of EHEC, and approximately 75% of EHEC outbreaks are linked to the consumption of contaminated bovine-derived products. This review will discuss how EHEC causes disease in humans but is asymptomatic in adult ruminants. It will also analyze factors utilized by EHEC as it travels through the bovine gastrointestinal tract that allow for its survival through the acidic environment of the distal stomachs, and for its ultimate colonization in the recto-anal junction. Understanding the factors crucial for EHEC survival and colonization in cattle will aid in the development of alternative strategies to prevent EHEC shedding into the environment and consequent human infection.

Enterohemorrhagic Escherichia coli O157:H7 infects about 73,000 people annually in the USA and is a major cause of outbreaks of bloody diarrhea worldwide, and. In 5 to 7% of the cases, the person infected develops the potentially fatal sequelae hemolytic uremic syndrome (HUS), characterized by acute kidney failure. A hallmark of EHEC pathogenesis and cause of HUS is the production of Shiga toxin (Stx). Stx was first described by Kiyoshi Shiga in Shigella dysenterae serotype I and later discovered in EHEC, and it has been linked to HUS since 1983. Many factors regulate the production of Stx, including temperature, growth phase, antibiotics, reactive oxygen species and quorum sensing. Currently, there is no effective treatment or prophylaxis for HUS. Since the use of antibiotics is not advised to treat EHEC infections because it triggers Stx production, alternative antibacterial strategies need to be developed. Quorum sensing inhibitors represent a novel class of antibacterial compounds, which have the advantage of not interfering on bacterial growth, thereby without selective pressure that can lead to appearance of resistant strains. In this review, we discuss factors that regulate Stx production in EHEC as well as novel strategies to fight Stx and minimize development to HUS in EHEC-infected patients.