Enterohaemorrhagic Escherichia coli O26:H11/H-:: A human pathogen in emergence

Enterolhaemorrhagic Escherichia coli (EHEC) 026:H11 have emerged as the most important non-O157:H7 EHEC, with respect to their ability to cause diarrhoea and the haemolytic uraemic syndrome (HUS). HUS is a leading cause of acute renal failure in children, and is mainly caused by EHEC expressing Shiga toxins (Stx) 1 and/or 2. Since 1996, EHEC 026, which produce Stx2 only and appear to have enhanced virulence, have been increasingly isolated from HUS patients in Germany. In contrast, EHEC 026 found in cattle predominantly produce Stx1 as the sole Stx. Additional potential virulence factors of EHEC 026 include cytolysins (EHFC hemolysin), serine proteases (EspP), lymphotoxins (Efa1) and adhesins (intimin). The genes encoding the virulence factors are located within pathogenicity islands (eae, efa1), bacteriophages (stx) or plasmids (EHEC-hlyA, espP). In addition, EHEC 026 possess, in contrast to other EHEC, the "high pathogenicity island" (HPI), which is also present in pathogenic Yersiniae. This island contains genes involved in the biosynthesis, regulation and transport of the siderophore yersiniabactin. Comparative genomic analyses between EHEC 026 and non-pathogenic E coli, as well as investigations of mechanisms involved in the transfer of virulence genes, provide a deeper insight into the evolution of EHEC 026. These studies demonstrate how horizontal transfer of virulence genes, even from distantly related organisms, can lead in brief intervals to the rise of a highly virulent clone within a particular E. coli serotype. The classical bacteriological methods are no longer sufficient to determine the risk posed by EHEC 026. However, knowledge of the complete virulence profiles of these pathogens and understanding their stepwise evolution form a foundation for developing new strategies to prevent human infections and new methods for their laboratory diagnosis.