Abstract
Shiga toxin-producing Escherichia coli (STEC) is a pathogen that causes gastroenteritis and bloody diarrhea but can lead to severe disease, such as hemolytic uremic syndrome (HUS). STEC serotype O78:H(-) is rare among humans, and infections are often asymptomatic. We detected a sorbitol-fermenting STEC O78:H(-):stx(1c):hlyA in blood and fecal samples of a 2-week-old boy who had bacteremia and HUS and in fecal samples of his asymptomatic family members. The phenotypic and genotypic characteristics and the virulence properties of this invasive STEC were investigated. Our findings demonstrate that contrary to earlier suggestions, STEC under certain conditions can invade the human bloodstream. Moreover, this study highlights the need to implement appropriate diagnostic methods for identifying the whole spectrum of STEC strains associated with HUS.
Highlights
Diarrheagenic Escherichia coli strains, Shiga toxin–producing E. coli (STEC), are foodborne and waterborne pathogens that cause a wide spectrum of symptoms, ranging from mild gastroenteritis to severe diseases such as hemorrhagic colitis, thrombotic thrombocytopenic purpura, and hemolytic uremic syndrome (HUS) [1]
The 6 strains isolated from the blood and fecal samples of the neonate and from the fecal samples of his asymptomatic parents and 2 siblings showed a sorbitolfermenting Shiga toxin–producing Escherichia coli (STEC) serotype O78:H– that carried the virulence genes stx1 and hlyA (Table)
The main cause for uremia in neonates with urosepsis is acute tubular necrosis. In this case, the signs fulfilled the criteria for D+ HUS and was associated with a family cluster of STEC O78:H
Summary
Diarrheagenic Escherichia coli strains, Shiga toxin–producing E. coli (STEC), are foodborne and waterborne pathogens that cause a wide spectrum of symptoms, ranging from mild gastroenteritis to severe diseases such as hemorrhagic colitis, thrombotic thrombocytopenic purpura, and hemolytic uremic syndrome (HUS) [1]. The colonization mechanism for the cell invasion is not yet fully understood, but the bacterium is known to attach firmly to the epithelial cells through an outer membrane protein called intimin This protein is encoded by the gene eae on a pathogenicity island called the locus of enterocyte effacement, and the bacterial fimbriae are presumed to be involved in the process [6]. HUS is characterized by acute onset of microangiopathic hemolytic anemia, renal injury, and low platelet count [7] It is primarily a disease of infancy and early childhood because infants and young children are more vulnerable than adults, even for low Stx concentrations; humans of all ages can be affected. Some sorbitol-positive strains of non–O157 STEC serotypes cause a similar spectrum of signs and symptoms [9]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
