Abstract
Shiga toxin-producing Escherichia coli (STEC) are able to cause serious illnesses ranging from diarrhea to hemorrhagic colitis and hemolytic-uremic syndrome (HUS). These bacteria colonize the digestive tract of humans and produce Shiga-toxins, which are considered to be essential for virulence and are crucial in lethal infection. Colon colonization is supposed to be a determinant step in the development of the infection, but the virulence traits that mediate this step are unclear. We analyzed the ability of 256 STEC strains belonging to seropathotype A (the most virulent O157:H7 serotype) to seropathotype E (not involved in human disease) to adhere to HEp-2, HCT-8, and T84 cell lines. Of the 256 STEC tested most (82%) were non-adherent in our assays. The adhesion levels were globally low and were not related to pathogenicity, although the highest levels were associated to O26:H11 and O103:H2 strains of seropathotype B (associated with HUS but less commonly than serotype O157:H7), possessing both the eae and toxB genes.
Highlights
Shiga toxin (Stx)-producing Escherichia coli (STEC) can be associated with human diseases, ranging from uncomplicated diarrhea to hemorrhagic colitis (HC) and hemolytic-uremic syndrome (HUS; Hussein, 2007)
Quantitative experiments, performed on 17 Shiga toxin-producing Escherichia coli (STEC) strains isolated from human cases, indicated that the number of bacteria adhering to the T84 cells was between 2.4 × 103 and 4.4 × 105 CFU/well (Figure 2A)
We analyzed the adhesion properties of a collection of 256 STEC strains isolated from cattle, food, and humans, using the intestinal epithelial cell lines HCT-8, T84, and the HEp-2 cells from human larynx carcinoma
Summary
Shiga toxin (Stx)-producing Escherichia coli (STEC) can be associated with human diseases, ranging from uncomplicated diarrhea to hemorrhagic colitis (HC) and hemolytic-uremic syndrome (HUS; Hussein, 2007). An outbreak with 1000s cases of food-borne illness has been caused by an emerging atypical O104:H4 Stx-producing pathogen in 2011 in Germany (Bielaszewska et al, 2011; Frank et al, 2011; Clements et al, 2012; Trachtman et al, 2012). Several studies have shown a high prevalence of STEC belonging to a wide range of serotypes in animals and food products (Pradel et al, 2000; Beutin, 2006; Hussein, 2007). The known virulence factors do not allow differentiation of STEC strains with a high pathogenic potential from their counterparts of lesser clinical significance
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