Healthy gut bacteria protects against E. coli O157:H7

Tuesday, 28 May, 2013

Having healthy gut bacteria could mean the difference between life and death, new research from the University of Michigan Medical School suggests.

Mice that were pre-colonised with a mix of bacterial species from normal human intestines remained completely healthy when infected with enterohemorrhagic Escherichia coli (EHEC) O157:H7, while those with uncolonised guts developed kidney disease and showed high levels of Shiga toxins (Stx) within one week of infection.

EHEC is a food-borne pathogen that has been responsible for several recent outbreaks of potentially fatal disease. Severe manifestations of this disease include hemorrhagic colitis (HC) and haemolytic uremic syndrome (HUS), a form of acute renal disease that can result in death or permanent disability.

“EHEC is of primary concern because HUS, the most severe outcome, preferentially targets young children,” said Kathryn Eaton, a researcher involved in the study. “Tragically, HUS occurs late in the course of disease, often after the child has recovered from the enteric form. Thus, children who appear to have recovered may relapse and even die.”

HUS is caused by absorption of Shiga toxins that are produced by the bacteria in the intestine. Stx production occurs within a few days of bacterial colonisation and once it is present in the intestines it can be absorbed into the bloodstream where it may cause systemic disease and even death. There is no specific treatment or preventative measure that prevents progression from HC to HUS.

“In brief, the results of our study show that in a mouse model, non-pathogenic bacteria that are normal inhabitants of the human intestine can eliminate Stx from the intestinal contents and completely prevent HUS,” said Eaton.

“The discovery that normal intestinal bacteria can prevent intestinal Stx accumulation and disease in an animal model may have important implications for prevention of HUS in people infected with EHEC.”

The research was presented at the 113th General Meeting of the American Society for Microbiology.

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