May 14, 2010

US study focuses on mechanism to stop E. coli development in cattle

Microbiologists at UT Southwestern Medical Centre in the US, working with the USDA, have identified a potential target in cattle that could be exploited to help prevent outbreaks of foodborne illnesses caused by E. coli.

In the study, researchers interfered with a genetic sensing mechanism that allows the E. coli strain known as enterohemorrhagic O157:H7 (EHEC), to form colonies within cattle, causing the bacteria to die off before they could reach the animals' recto-anal junction, the primary site of colonisation. Most other strains of E coli gather in the colon.

"We're diminishing colonisation by not letting EHEC go where it needs to go efficiently," said Dr Vanessa Sperandio, associate professor of microbiology and biochemistry at UT Southwestern and senior author of the study. "If we can find a way to prevent these bacteria from colonising in cattle, it's possible that we can have a real impact on human disease," she said.

"This could be something as simple as including some sort of antagonist in cattle feed, which would result in less shedding of the bacteria in faecal matter with less contamination down the road in food products," said Dr Sperandio. This finding is important because an estimated 70-80% of the cattle herds in the US carry EHEC.

Although EHEC can be a deadly pathogen to humans, the bacterium is part of cattle's normal gastrointestinal flora. EHEC harbours a gene called sdiA, which makes the SdiA protein. The SdiA protein senses a chemical made by microbes in the animal's rumen, the first of a cow's four stomachs, which serves as a large fermentation chamber. Detecting this signal allows EHEC to pass through the rumen and colonise the recto-anal junction.

For the study, the researchers injected two types of EHEC into the rumens of eight grain-fed adult cows. One mutant version lacked SdiA and could not detect the signal in the rumen. Another strain produced an enzyme that destroyed the chemicals in the rumen sensed by SdiA. The researchers found that colonisation diminished significantly when these EHEC strains were unable to sense the rumen chemicals. The process prevented the bacteria from moving on through the stomach and colonising.

"If there's no signal, then there's no acid resistance, a requirement for the pathogen to make it to the recto-anal junction," Dr Sperandio said. "Everybody had thought that this type of signalling occurred naturally in the gastrointestinal tract of mammals. Our finding serves as a proof-of-principle that we might be able to target this system to prevent food contamination for humans."