Authors:
Kakolie Goswami, Chun Chen, Lingzi Xiaoli, Kathryn A. Eaton, and Edward G. Dudley
Summary:
E. coli O157:H7 is a notorious foodborne pathogen due to its low infectious dose and disease symptoms that include bloody diarrhea and severe abdominal cramps. In some cases, the disease progresses to hemorrhagic colitis (HC) and hemolytic uremic syndrome (HUS), due to the expression of one or more Shiga toxins (Stx). Isoforms of Stx, including Stx2a, are encoded within temperate prophages. In the presence of certain antibiotics phage induction occurs, which also increases expression of toxin genes. Additionally, increased Stx2 accumulation was reported when O157:H7 was co-cultured with phage-susceptible non-pathogenic E. coli. This study characterized an E. coli O157:H7 strain, designated as PA2, which belongs to the hypervirulent clade 8 cluster. Stx2a levels after ciprofloxacin induction were lower for PA2 compared to prototypical outbreak strains Sakai and EDL933. However, during co-culture with the non-pathogenic strain E. coli C600, PA2 produced Stx2a levels that were two to 12-fold higher than those observed during co-culture with Sakai and EDL933, respectively. Germ-free mice co-colonized by PA2 and C600 showed greater kidney damage, increased Stx2a accumulation in feces, and more visible signs of disease than mice given PA2 or C600 alone. These data suggest one mechanism by which microorganisms associated with the colonic microbiota could enhance the virulence of E. coli O157:H7, particularly a subset of clade 8 strains.
Source:
Infection & Immunity; (08/10/15)