Purpose: To determine the distribution of pathogenicity islands among STEC O26, O103, and O111.
Methods: A collection of STEC O26 (n = 45), O103 (n = 48), and O111 (n = 52) from humans and animals were included in this study. Pulsed-field gel electrophoresis (PFGE) with XbaI digestion was used to characterize the clonal relationship of the strains. In addition, a PCR-RFLP assay was used to determine eae subtypes. Additional virulence genes on PAIs were identified using specific PCR assays, including OI-122: pagC, sen, efa-1, efa-2, and nleB ; OI-43/48: terC, ureC, iha, and aidA-1; OI-57: nleG2-3, nleG5-2, and nleG6-2; and HPI: fyuA, and irp2.
Results: The strains of the same serotypes tend to have identical PAI patterns regardless of source except OI-43/48 in O103:H2 (P < 0.05). PFGE dendrogram demonstrated that instead of clustering together with strains from same O type (O111:H8), the O111:H11 (n=16) strains tended to be clustered together with strains of the same H type (O26:H11, n=45). In addition, O26:H11 and O111:H11 strains carried eae subtype beta, whereas O111:H8 strains had eae gamma2/theta. The O26:H11 and O111:H11 stains contained an incomplete OI-122 lacking pagC and a complete HPI. However, a complete OI-122 but no HPI was found in the O111:H8 strains. Additionally, aidA-1of OI-43/48 and nleG6-2 of OI-57 were significantly associated with O26:H11 and O111:H11 strains but were almost missing in O111:H8 strains (P< 0.001).
Significance: This study demonstrated that H11 (O111:H11 and O26:H11) strains were closely related and may have come from the same ancestor. H antigen might be used as a valuable marker to predict virulence potential and evolutional relationship of non-O157 STEC in combination with other markers.