Abstract
Escherichia coli O157:H7 is a food-borne bacterium that causes hemorrhagic diarrhea and hemolytic uremic syndrome in humans. While cattle are a known source of E. coli O157:H7 exposure resulting in human infection, environmental reservoirs may also be important sources of infection for both cattle and humans. Bacteriophage-encoded Shiga toxins (Stx) carried by E. coli O157:H7 may provide a selective advantage for survival of these bacteria in the environment, possibly through their toxic effects on grazing protozoa. To determine Stx effects on protozoan grazing, we co-cultured Paramecium caudatum, a common ciliate protozoon in cattle water sources, with multiple strains of Shiga-toxigenic E. coli O157:H7 and non-Shiga toxigenic cattle commensal E. coli. Over three days at ambient laboratory temperature, P. caudatum consistently reduced both E. coli O157:H7 and non-Shiga toxigenic E. coli populations by 1–3 log cfu. Furthermore, a wild-type strain of Shiga-toxigenic E. coli O157:H7 (EDL933) and isogenic mutants lacking the A subunit of Stx 2a, the entire Stx 2a-encoding bacteriophage, and/or the entire Stx 1-encoding bacteriophage were grazed with similar efficacy by both P. caudatum and Tetrahymena pyriformis (another ciliate protozoon). Therefore, our data provided no evidence of a protective effect of either Stx or the products of other bacteriophage genes on protozoan predation of E. coli. Further research is necessary to determine if the grazing activity of naturally-occurring protozoa in cattle water troughs can serve to decrease cattle exposure to E. coli O157:H7 and other Shiga-toxigenic E. coli.
Highlights
Diseases caused by the bacterium Escherichia coli O157:H7 are major public health concerns worldwide, with the highest numbers of reported cases in the United States, United Kingdom, Argentina, Canada and Japan [1, 2]
We evaluated the ability of protozoa to graze diverse genotypes of Shiga-toxigenic E. coli O157:H7 over three days using cattle water trough isolates of the protozoon, Paramecium caudatum
We evaluated the ability of protozoa to graze E. coli O157:H7 strain EDL933 and isogenic mutants with deletion of the Stx2a subunit A-encoding nucleotide sequence, deletion of the entire Shiga toxins (Stx) 2a-encoding bacteriophage sequence, and/or deletion of the entire Stx1-encoding bacteriophage sequence, using both P. caudatum and the laboratory strain of T. pyriformis previously described as susceptible to Stx [14]
Summary
Diseases caused by the bacterium Escherichia coli O157:H7 are major public health concerns worldwide, with the highest numbers of reported cases in the United States, United Kingdom, Argentina, Canada and Japan [1, 2]. Protozoa Graze Escherichia coli O157:H7 effacement (LEE) pathogenicity island and one or more Shiga toxins (Stx), primarily Stx, Stx2a, and Stx2c. The LEE pathogenicity island is responsible for attaching and effacing lesions seen in both humans and cattle. Stx targets endothelial cells in the colon contributing to hemorrhagic colitis [5], and renal glomerular endothelial cells in some cases resulting in the life-threatening disease, hemolytic uremic syndrome (HUS) [6, 7]
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