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ARS Home » Northeast Area » Wyndmoor, Pennsylvania » Eastern Regional Research Center » Characterization and Interventions for Foodborne Pathogens » Research » Publications at this Location » Publication #296332
Title: Shiga toxin-producing Escherichia coli

Author
item SMITH, JAMES
item Fratamico, Pina
item Gunther, Nereus - Jack

Submitted to: Advances in Applied Microbiology
Publication Type: Book / Chapter
Publication Acceptance Date: 7/30/2013
Publication Date: 1/21/2014
Citation: Smith, J.L., Fratamico, P.M., Gunther, N.W. 2014. Shiga toxin-producing Escherichia coli. Advances in Applied Microbiology. 86:145-197.

Interpretive Summary:

Technical Abstract: In United States, it is estimated that non-O157 Shiga toxin-producing Escherichia coli (STEC) cause more illnesses than STEC O157:H7, and the majority of cases of non-O157 STEC infections is due to serogroups O26, O45, O103, O111, O121, and O145, referred to as the top six non-O157 STEC. The diseases caused by non-O157 STEC are generally milder than those induced by O157 STEC; nonetheless, non-O157 STEC strains have also been associated with serious illnesses such as hemorrhagic colitis and hemolytic uremic syndrome, as well as death. Ruminants, particularly cattle, are reservoirs for both O157 and non-O157 STEC, which are transmitted to humans by person-to-person or animal contact and by ingestion of food or water contaminated with animal feces. Improved strategies to control STEC colonization and shedding in cattle and contamination of meat and produce are needed. In general, non-O157 STEC respond to stresses such as acid, heat, and other stresses induced during food preparation similar to O157 STEC. Similar to O157:H7, the top six non-O157 STEC are classified as adulterants in beef by the USDA Food Safety and Inspection Service, and regulatory testing for these pathogens began in June, 2012. Due to the genetic and phenotypic variability of non-O157 STEC strains, the development of accurate and reliable methods for detection and isolation of these pathogens has been challenging. Since the non-O157 STEC are responsible for a large portion of STEC-related illnesses, more extensive studies on their physiology, genetics, pathogenicity, and evolution are needed in order to develop more effective control strategies.