Background: Hemolytic uremic syndrome (HUS) has been associated with typhoid fever caused by Salmonella typhi. The pathogenesis of HUS in the context of S typhi infection is not known. The authors report on a patient with typhoid fever in whom HUS and myocarditis developed during the course of his illness and in whom there was no evidence of a Shiga-toxin (Stx)-producing organism.

Methods: Antibodies directed against the Escherichia coli O157:H7 and S typhi lipopolysaccharide (LPS) were sought in the serum sample taken during the acute phase using line-blot immunoassays. Polymerase chain reaction was performed to detect the presence of stx1 and stx2 genes in the patient's S typhi isolate.

Results: There was no evidence for immunoglobulin (Ig) M and IgA against the LPS of E coli O157:H7, whereas anti-S typhi LPS IgM and IgA were strongly positive. In the polymerase chain reaction, DNA from the Stx-producing E coli controls yielded stx1 and stx2 fragments of the expected sizes on agarose gel electrophoresis, whereas no stx1 and stx2 fragments were obtained from the S typhi isolate. The S typhi did, however, yield a band when amplified with primers specific for viaB, an S typhi gene.

Conclusions: S typhi may be responsible for some cases of HUS, and the inciting toxin may not be Stx.