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About the Authors:
Kjersti Haugum
* E-mail: [email protected]
Affiliation: Department of Laboratory Medicine, Children’s and Women’s Health, Faculty of Medicine, Norwegian University of Science and Technology, Trondheim, Norway
Jostein Johansen
Affiliation: Department of Cancer Research and Molecular Medicine, Faculty of Medicine, Norwegian University of Science and Technology, Trondheim, Norway
Christina Gabrielsen
Affiliation: Department of Laboratory Medicine, Children’s and Women’s Health, Faculty of Medicine, Norwegian University of Science and Technology, Trondheim, Norway
Lin T. Brandal
Affiliation: Department of Foodborne Infections, Norwegian Institute of Public Health, Oslo, Norway
Kåre Bergh
Affiliations Department of Laboratory Medicine, Children’s and Women’s Health, Faculty of Medicine, Norwegian University of Science and Technology, Trondheim, Norway, Department of Medical Microbiology, St. Olavs University Hospital, Trondheim, Norway
David W. Ussery
Affiliation: Biosciences Division, Oak Ridge National Labs, Oak Ridge, Tennessee, United States of America
Finn Drabløs
Affiliation: Department of Cancer Research and Molecular Medicine, Faculty of Medicine, Norwegian University of Science and Technology, Trondheim, Norway
Jan Egil Afset
Affiliations Department of Laboratory Medicine, Children’s and Women’s Health, Faculty of Medicine, Norwegian University of Science and Technology, Trondheim, Norway, Department of Medical Microbiology, St. Olavs University Hospital, Trondheim, Norway
Introduction
Shiga toxin producing E. coli (STEC) are important human pathogens known to cause infections ranging from diarrhoea and haemorrhagic colitis to haemorrhagic uremic syndrome (HUS) [1]. Since the first reports of disease caused by O157:H7 in 1982 [2], [3], this serotype has been the most frequently reported cause of severe STEC disease and outbreaks worldwide [1]. However, several non-O157 STEC serogroups (e.g. O26, O45, O103, O111, O121 and O145) have also been recognized to be responsible for severe disease and outbreaks [4], [5].
The STEC pathotype is defined by the presence of Shiga toxins Stx1 and Stx2 encoded by the stx1 and stx2 genes, which are acquired through horizontal gene transfer of a heterogeneous group of lambdoid bacteriophages [6]–[9]. There are several subtypes of Shiga toxins, of which the Stx2 subtypes Stx2a, Stx2c and Stx2d are more often associated with HUS than other Stx subtypes [10]–[13]. In addition, the adherence factor intimin, encoded by the eae gene located in the Locus of Enterocyte Effacement (LEE) pathogenicity island, is important for STEC pathogenicity. STEC causing severe disease and outbreaks do usually harbour LEE [1],...