Associations between Virulence Factors of Shiga Toxin-ProducingEscherichia coliand Disease in Humans

Abstract

Associations between known or putative virulence factors of Shiga toxin-producing Escherichia coli and disease in humans were investigated. Univariate analysis and multivariate logistic regression analysis of a set of 237 isolates from 118 serotypes showed significant associations between the presence of genes for intimin (eae) and Shiga toxin 2 (stx 2) and isolates from serotypes reported in humans. Similar associations were found with isolates from serotypes reported in hemorrhagic colitis and hemolytic-uremic syndrome. The enterohemorrhagic E. coli (EHEC) hemolysin gene was significantly associated with isolates from serotypes found in severe diseases in univariate analysis but not in multivariate logistic regression models. A strong association between the intimin and EHEC-hemolysin genes may explain the lack of statistical significance of EHEC hemolysin in these multivariate models, but a true lack of biological significance of the hemolysin in humans or in disease cannot be excluded. This result warrants further investigations of this topic. Multivariate analysis revealed an interaction between the eae andstx 2 genes, thus supporting the hypothesis of the synergism between the adhesin intimin and Shiga toxin 2. A strong statistical association was observed between thestx 2 gene and severity of disease for a set of 112 human isolates from eight major serotypes. A comparison of 77 isolates of bovine origin and 91 human isolates belonging to six major serotypes showed significant associations of the genes for Shiga toxin 1 and EspP protease with bovine isolates and an increased adherence on HEp-2 cell cultures for human isolates, particularly from diarrheic patients and healthy persons.

Characterization of Shiga toxin-producingEscherichia coliisolated from aquatic environments

“…The presence of the stx 2 gene in the infecting strain was previously reported to correlate with severe disease in humans [28,32] and the administration of purified Stx 2 , but not of Stx 1 , was shown to cause HUS in experimentally treated primates [33]. Six genetic variants of stx 2 have been detected by nucleotide sequence analysis: stx 2 , stx 2c , stx 2d , stx 2e , stx 2f and stx 2g .…”

Target genes for virulence assessment of Escherichia coli isolates from water, food and the environment

“…They include attachment functions, host cell surface modifying factors, invasins, and many di¡erent toxins as well as secretion systems which export toxins and other virulence factors and pilot them to the target host cells. The term`virulence factor' is actually not precisely de¢ned since a single component might not be su¤cient to transform an E. coli strain into a pathogenic one but could only play a role in combination with other (virulence) determinants [26,27]. In the present review we use the term`virulence factor' for determinants that have a major contribution to a strain's pathogenic potential.…”

Shiga Toxin-Producing Escherichia coli O104:H4: a New Challenge for Microbiology

“…In HUS, the main affected organs are the kidney and the brain, but other organs can also be involved (23). HUS is mostly associated with EHEC strains producing Stx2 and/or Stx2c (9). Because renal glomerular capillary thrombotic microangiopathy is the hallmark of EHEC-associated HUS, the cytotoxicity of Stx is probably directly linked to the pathogenesis of HUS (40).…”