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To the Editor—Johnson [1] makes the important points that the specificity of serologic assays varies with the population studied and that serologic results can be interpreted only when that specificity is known. Although control subjects without a diarrheal illness were used in determining the positive cutoff values in our original description of the assay we used [2], the assay has since been validated with serum from patients having other diarrheal illnesses, including non–O157 Shiga toxin–producing Escherichia coli (STEC) infections

During investigations of outbreaks and clusters of cases caused by STEC serogroups O104 [3], O111 [4], and O121 (authors’ unpublished data) and sporadic cases of hemolytic uremic syndrome (HUS) caused by serogroups O79, O86, and O103 (authors’ unpublished data), we saw minimal reactivity of patient serum with E. coli O157 lipopolysaccharide (LPS). Ludwig et al. [5], using a similar test, found no reactivity with O157 LPS in serum from patients with HUS caused by STEC serogroups O55 and O111 but found apparent cross-reactivity in one of 3 serum samples from HUS patients infected with STEC serogroup O26. When Chart et al. [6] examined cross-reactivity of O157 LPS with hyperimmune antisera to a variety of organisms, only group N Salmonella and Vibrio cholerae O1 Inaba were found to share epitopes with E. coli O157 LPS. Other organisms that share epitopes with O157 LPS include Brucella, Yersinia enterocolitica, Citrobacter freundii and E. hermanii [7]. Either infection with these organisms is very rare in the United States, or the clinical presentation is not consistent with HUS

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