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Gut infection regulator identified

12 September 2007

Dr Dena Lyras and Dr Glen Carter have found a new gene that regulates toxin production in an endemic, human-gut disease.

Scientists in the School of Biomedical Sciences have found a gene that controls toxin production in an endemic, human-gut disease.

Dr Glen Carter and Dr Dena Lyras, working in Professor Julian Rood's laboratory in the Department of Microbiology in the School of Biomedical Sciences, have found a new gene that regulates toxin production in the bacterium Clostridium difficile, which can cause gastrointestinal intestinal disease syndromes known as C. difficile associated disease (CDAD).

CDAD is the most commonly diagnosed bacterial cause of infectious hospital- acquired diarrhoea in developed countries. In severe cases it can result in death.

The incidence of CDAD has been steadily increasing, especially among the elderly and children.

Dr Carter said in the UK, US and Canada, scientists had seen the emergence of a new hypervirulent strain of C. difficile that results in a higher-than-average mortality rate, and the closure of entire hospital wards.

C. difficile produces three known toxins, but until this research was carried out little was known about how the expression of one of these toxins was regulated.

"Identifying the regulatory gene is the first step towards understanding it. It gives us an extra target to work with to try and shut off the toxins that cause infection," Dr Carter said.

The onset of the infection is associated with the use of antibiotics that disrupt the usual intestine environment, enabling C. difficile spores from the environment to colonise the gut and cause diarrhoea.

"We know that the toxin regulated by this regulatory protein is not essential for the development of the disease because not all C. difficile strains produce the toxin," Dr Lyras said.

"Our next step is to work out exactly what it does. If we can understand how C. difficile produces the toxin, we can work towards trying to prevent its expression."