Shiga Toxin in Enterohemorrhagic E.coli: regulation and novel antivirulence strategies

• Published in: Frontiers in cellular and infection microbiology Vol. 2
• Main Authors: Vanessa eSperandio, Alline Roberta Pacheco
• Format: Journal Article
• Language: English
• Published: Frontiers Media S.A 01.06.2012
• Subjects: enterohemorrhagic E. coli (EHEC); hemolytic uremic syndrome (HUS); Shiga Toxin
• ISSN: 2235-2988
• DOI: 10.3389/fcimb.2012.00081

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.