ABO and P1 blood group antigen expression and stx genotype and outcome of childhood Escherichia coli
ABO and P1 blood group antigen expression and stx genotype and outcome of childhood Escherichia coli O157:H7 infections. Jelacic S, Wobbe CL, Boster DR, Ciol MA, Watkins SL, Tarr PI, Stapleton AE. The Journal of Infectious Diseases 2002;185:214-219.
Hemolytic uremic syndrome (HUS) is a thrombogenic microangiopathy believed to be precipitated by Shiga toxin (Stx) absorbed from the gut and produced by Escherichia coli O157:H7. Various red blood cell antigens have been proposed to either play a role in the development of Stx-mediated HUS or modulate the severity of resulting HUS, such the P1 antigen and B blood group antigen. The comparative virulence of Stx1 and 2 have also been proposed to affect disease outcome in E. coli O157:H7 infections, with Stx2 considered more potent. This study analyzed risk factors for the development of HUS after E. coli O157:H7 infections, specifically the expression of blood type and the P1 antigen in the patient and Stx genotype of the infection strain. Samples from 148 children less than 10 years of age in the U.S. Pacific Northwest were studied. These included 106 with uncomplicated infection and 25 with HUS, plus 17 control subjects. There was no difference between these groups in the distribution of the P1 blood group antigen, and no association was found between ABO blood group and HUS development. Stx1 negative/Stx2 positive E. coli O157:H7 were more frequently isolated than Stx1 positive/Stx2 positive E. coli O157:H7 from subjects with HUS than from those with uncomplicated infection, but this difference was not statistically significant. In an analysis that took into account Stx, ABO, and P1, only P1 was significantly associated with the development of HUS by an infected host. It is difficult to draw conclusions, however, because only the group positive at the 3+ level, but not at the higher or lower levels was observed to be associated with HUS risk. The authors conclude that ABO antigens and Stx genotypes were not major determinants of HUS, and P1 expression did not protect against the development of HUS.