Shiga-like toxin (SLT) plays an important role in the etiology of HUS. Infection with the SLT producing enteric pathogen E. coli O157:H7 causes 90% of childhood HUS. Infection with other bacterial pathogens such as Salmonella has also preceded HUS episodes, leading to speculation that these organisms either produce SLT or cause HUS via another etiologic pathway. Recently we treated two children, aged 2 and 6 years, with unrelated cases of classic HUS, Salmonella enteritis and immune response to E. coli O157:H7. Pertinent clinical and laboratory data are listed in the table. Both patients had negative stool cultures on sorbitol-MacConkey agar soon after onset of symptoms. After diagnosis of HUS, repeat stool cultures revealed Salmonella alone. Polymerase chain reactions for SLT I and II gene sequences in both Salmonella isolates were negative. ELISA for specific humoral response to E. coli O157:H7 lipopolysaccharide in acute and convalescent serum samples revealed heretofore undetected E. coli infection contemporaneous with each HUS episode. We conclude: 1) Isolation of only non-SLT producing microbes in a child with HUS should raise suspicion for concurrent undetected infection with SLT producing organisms; 2) Assaying specific immune response to E. coli O157:H7 may be an important epidemiologic adjunct in determining HUS-inciting infection; and 3) Bacterial infection with non-SLT producing Salmonella may represent concomitant enteric pathology rather than HUS-instigating infection.

Table 1
Full size table