Abstract
Escherichia coli O157:H7 is the predominant cause of diarrhea-associated hemolytic uremic syndrome (HUS) worldwide. Its cardinal virulence traits are Shiga toxins, which are encoded by stx genes, the most common of which are stx1a, stx2a, and stx2c. The toxins these genes encode differ in their in vitro and experimental phenotypes, but the human population-level impact of these differences is poorly understood. Using Shiga toxin-encoding bacteriophage insertion typing and real-time polymerase chain reaction, we genotyped isolates from 936 E. coli O157:H7 cases and verified HUS status via chart review. We compared the HUS risk between isolates with stx2a and those with stx2a and another gene and estimated additive interaction of the stx genes. Adjusted for age and symptoms, the HUS incidence of E. coli O157:H7 containing stx2a alone was 4.4% greater (95% confidence interval (CI) −0.3%, 9.1%) than when it occurred with stx1a. When stx1a and stx2a occur together, the risk of HUS was 27.1% lower (95% CI −87.8%, −2.3%) than would be expected if interaction were not present. At the population level, temporal or geographic shifts toward these genotypes should be monitored, and stx genotype may be an important consideration in clinically predicting HUS among E. coli O157:H7 cases.
Highlights
Escherichia coli O157:H7 is a leading cause of hospitalization for foodborne illness and the predominant cause of post-diarrheal hemolytic uremic syndrome (HUS) [1]
Its cardinal virulence factor, namely Stx1 and Stx2. These toxins are encoded by several allelic variants, of which stx1a, stx2a, and stx2c are most common among E. coli O157:H7 strains isolated from humans
After reassigning the genotype of the isolates that might have lost an stx gene after isolation, the excess risk associated with the stx2a-only genotype was similar or marginally in excess of that seen in the primary analysis
Summary
Escherichia coli O157:H7 is a leading cause of hospitalization for foodborne illness and the predominant cause of post-diarrheal hemolytic uremic syndrome (HUS) [1]. Characterized by hemolytic anemia, thrombocytopenia, and renal injury, HUS often necessitates renal replacement. Toxins 2019, 11, 607 therapy, has a 1–5% case fatality [2,3,4], and is believed to be the consequence of vascular injury from circulating Shiga toxins (Stx) produced by this pathogen [5]. Children
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