Main content area

Dietary choice affects Shiga toxin-producing Escherichia coli (STEC) O157:H7 colonization and disease

Zumbrun, Steven D., Melton-Celsa, Angela R., Smith, Mark A., Gilbreath, Jeremy J., Merrell, D. Scott, O’Brien, Alison D.
Proceedings of the National Academy of Sciences of the United States of America 2013 v.110 no.23 pp. E2126
Escherichia coli O157, Shiga toxin, body weight, butyrates, disease severity, food choices, food pathogens, hemolytic uremic syndrome, high fiber diet, ingestion, intestinal microorganisms, intestines, low fiber diet, mice, morbidity, mortality
The likelihood that a single individual infected with the Shiga toxin (Stx)-producing, food-borne pathogen Escherichia coli O157:H7 will develop a life-threatening sequela called the hemolytic uremic syndrome is unpredictable. We reasoned that conditions that enhance Stx binding and uptake within the gut after E. co li O157:H7 infection should result in greater disease severity. Because the receptor for Stx, globotriaosylceramide, is up-regulated in the presence of butyrate in vitro, we asked whether a high fiber diet (HFD) that reportedly enhances butyrate production by normal gut flora can influence the outcome of an E. coli O157 infection in mice. To address that question, groups of BALB/c mice were fed high (10%) or low (2%) fiber diets and infected with E . coli O157:H7 strain 86-24 (Stx2+). Mice fed an HFD exhibited a 10- to 100-fold increase in colonization, lost 15% more body weight, exhibited signs of morbidity, and had 25% greater mortality relative to the low fiber diet (LFD)-fed group. Additionally, sections of intestinal tissue from HFD-fed mice bound more Stx1 and expressed more globotriaosylceramide than did such sections from LFD-fed mice. Furthermore, the gut microbiota of HFD-fed mice compared with LFD-fed mice contained reduced levels of native Escherichia species, organisms that might protect the gut from colonization by incoming E. coli O157:H7. Taken together, these results suggest that susceptibility to infection and subsequent disease after ingestion of E. coli O157:H7 may depend, at least in part, on individual diet and/or the capacity of the commensal flora to produce butyrate.