Enterohemorrhagic E. coli (EHEC) are strains capable of producing Shiga toxin and typically cause bloody diarrhea [1-3]. Hemolytic-uremic syndrome complicates 6 to 9 percent of EHEC infections overall and about 15 percent of EHEC infections in children under age 10 [3-6]. Since the initial recognition of severe bloody diarrhea due to a new serotype of E. coli, O157:H7, in the United States in 1982, outbreaks and sporadic infections have been attributed to EHEC worldwide [4,5,7-22].
The microbiology, pathogenesis, epidemiology, and prevention of EHEC will be reviewed here. The clinical manifestations, diagnosis, and treatment of EHEC infections are discussed separately. (See "Clinical manifestations, diagnosis and treatment of enterohemorrhagic Escherichia coli (EHEC) infection".)
E. coli strains can be classified by their O and H antigens [23-25]. The O antigen is defined serologically and determined by the repeating polysaccharide chains that are part of the lipopolysaccharide (LPS) embedded in the outer leaflet of the outer membrane. The H antigen is defined serologically by the antigenic specificity of the bacterial flagellum.
EHEC strains of E. coli contain specific virulence properties: lysogenic phage encoding one or more Shiga toxins (with or without a chromosomal pathogenicity island), and often an additional virulence plasmid. These strains are also referred to as Shiga-toxin producing E. coli, or STEC.
In the United States, most EHEC strains are serotype O157:H7 . Non-O157 serotypes have also been described in the United States and in other countries; infections due to non-O157 serotypes are estimated to account for 30 to 50 percent of EHEC infections in the United States [21,26-28]. Among 940 human non-O157 STEC isolates submitted to the Centers for Disease Control (CDC) between 1983 and 2002, the most common serogroups were O26, O111, O103, O121, O45, and O145 (22, 16, 12, 8, 7, and 5 percent, respectively) .