Emerging hybrid shigatoxigenic and enteropathogenic Escherichia coli serotype O80:H2 in humans and calves

Abstract

SUMMARYAttaching-effacing (AE) lesion- and Shiga toxin-producing Escherichia (E.) coli (AE-STEC), previously known as "enterohemorrhagic E. coli" (EHEC), are responsible for (hemorrhagic) enterocolitis (HC) and hemolytic uremic syndrome (HUS) in humans. The most frequent and pathogenic AE-STEC belong to a few O:H major serotypes that are responsible for the majority of cases and outbreaks worldwide. From time to time, one or another non-major O:H serotype can emerge, causing either local outbreaks or a a progressive increase in clinical cases. One of these minor serotypes is O80:H2, which has been progressively emerging in Western Europe, especially in France, since 2010. AE-STEC O80:H2 are responsible for not only HC and HUS but also invasive infections with bacteremia and internal organ infection. In parallel to their emergence in humans, AE-STEC and enteropathogenic E. coli (EPEC) O80:H2 have also been emerging in young calves suffering diarrhea and enteritis and, more rarely septicemia, in Belgium since 2009. In this manuscript, an overview of AE-STEC and EPEC O80:H2 infections in humans and calves is presented, with particular focus on the clinical manifestations, the prevalence and incidence in Western Europe, and the identification of the potential reservoir(s). In addition, the results of a large-scale whole genome-based phylogenetic analysis of 417 published and unpublished genome sequences currently available in the literature and in the NCBI and EnteroBase databases are presented with hypotheses on the origin and evolution of this new hybrid AE-STEC and EPEC serotype.

Keywords: EPEC; Escherichia coli; O80:H2; STEC; bacteremia; calves; eae gene; evolution; hemolytic uremic syndrome; hemorrhagic colitis; humans; pR444_A plasmid; pS88 plasmid; phylogenetics; reservoir; septicemia; stx genes; virulotyping.