Submitted to: Current Issues in Intestinal Microbiology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: February 17, 2004
Publication Date: March 8, 2004
Citation: Callaway, T.R., Anderson, R.C., Edrington, T.S., Bischoff, K.M., Genovese, K.J., Poole, T.L., Harvey, R.B., Byrd II, J.A., Nisbet, D.J. 2004. Effects of sodium chlorate on toxin production by Escherichia coli O157:H7. Current Issues in Intestinal Microbiology. 5:19-22. Interpretive Summary: Escherichia coli O157:H7 is a food borne pathogenic bacterium that is killed by the addition of sodium chlorate. Toxin production by E. coli O157:H7 is dramatically increased when this bacterium is treated with traditional, medically-important antibiotics; thus causing a negative impact on human health. Because of this increase in toxin production, antibiotics are not recommended for use in human infections by E. coli O157:H7. This study demonstrates that chlorate does not increase toxin production by strains of E. coli O157:H7. This result indicates that chlorate could be used to treat a broad range of E. coli O157:H7 infections without fear of stimulating toxin production.
Technical Abstract: Chlorate kills E. coli O157:H7 and has been proposed as a feed additive to be included in cattle rations immediately prior to slaughter to reduce E. coli O157:H7 populations in the gut. Antibiotic usage is not recommended in cases of E. coli O157:H7-induced hemorrhagic colitis because some antibiotics stimulate toxin production. This study was undertaken to determine if chlorate treatment affected toxin production. Pure cultures of E. coli O157:H7 were treated with ¼ MIC of antibiotics (ampicillin, tetracycline, ceftiofur, gentamicin, monensin, tylosin, penicillin, ciprofloxacin, and novobiocin); toxin production was significantly increased by some antibiotics, but not by chlorate. Studies with mixed fecal bacteria demonstrated that chlorate killed E. coli O157:H7, but again did not stimulate toxin production. Chlorate appears to be an effective method to reduce shiga toxin-producing E. coli (STEC) populations in food animals, but additional studies are warranted before it is used to control infections.