Escherichia coli 0157:H7 causes diarrhea, hemorrhagic colitis, and the hemolytic uremic syndrome (HUS) [1, 2]. The cardinal virulence trait of E. coli 0157:H7 is the production of Shiga toxins (Stx, also termed Verocytotoxins) [3,4]. Unlike most coliforms in human feces, E. coli 0157:H7 does not ferment sorbitol after overnight incubation [5]. Therefore, it is easily and economically detected by laboratories using sorbitolMacConkey (s-Mac) agar screening to identify sorbitol-nonfermenting candidate E. coli 0157:H7 [6, 7]. Such colonies are then tested for the presence of the 0157 antigen, which, if detected, presumptively identifies Stx-producing E. coli (STEC) 0157:H7. In contrast, it is not known which of the many STEC belonging to serotypes other than 0157:H7 (non0157:H7 STEC) are pathogens; with rare exceptions [8, 9], such organisms ferment sorbitol and would be overlooked on an s-Mac agar plate. The same difficulty applies to the detection of sorbitol-fermenting Stx-producing E. coli 0157:NM, a pathogen in Germany [10]. In this issue, Ludwig et al. [11], report that 6 of 8 HUS patients from whom non-0157:H7 STEC were isolated produced antibodies to the O-specific lipopolysaccharide of the putatively causative strains. Ludwig et al. also determined that patients infected with E. coli expressing O antigens 26, 55, and 111 did not make antibodies to the 0157 lipopolysaccharide. Humans infected with E. coli 0157:H7 respond briskly with antibodies to the 0157 antigen [12-16], so absence of anti0157 antibodies probably exonerates E. coli 0157:H7 as the pathogen that precipitated the HUS. This is an important point, because children from whom such non-0157:H7 STEC have been isolated sometimes produce convalescent antibodies to the 0157 lipopolysaccharide [12-14], suggesting that E. coli 0157:H7 was missed in the stool culture. Furthermore, simultaneous enteric infections with E. coli 0157:H7 and non-