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Superbug debugged

An international team of scientists led by Monash researchers have uncovered how a superbug kills elderly patients worldwide. And, in doing so, they’ve upturned prevailing dogma. Of the two toxic proteins produced by the bacterium Clostridium difficile, they have shown that toxin B, not toxin A, causes intestinal disease.

For their efforts, team leader Professor Julian Rood and lead author Dr Dena Lyras from the Department of Microbiology have had their work published in the prestigious scientific journal Nature.

The research focuses on C. difficile, a superbug that infects hospital patients undergoing antibiotic therapy. The antibiotics destroy the ‘good’ bacteria in the gut and allow this ‘bad’ bacterium to thrive in the colon, where it triggers an immune response and chronic diarrhoea, which is difficult to treat.

In the US, more people die from C. difficile associated disease than all other intestinal infections combined, with most deaths involving people aged 65 years or over. It is estimated that it costs $3.2 billion each year (USD) to treat this disease in the US. If this superbug invades Australian hospitals and replaces less aggressive strains here, it will seriously threaten our healthcare system.

C. difficile produces two toxic proteins, toxins A and B. In their study, the Monash team constructed genetically-engineered mutants of C. difficile that produced only toxin A or toxin B. These modified organisms were then injected into animal models by colleagues in Chicago. The results showed that bugs that made toxin B still caused disease, unlike mutants that made toxin A. This disease causing protein is also detected in infected patients.

Why do these findings contradict earlier studies elsewhere? Dr Lyras explains: “We work with whole bacteria, which reflects what really happens in an infection, rather than working on purified toxins alone as most of our peers have done.”

“We’re also one of only three labs in the world that can do these complex experiments.”

Professor Rood agrees. “Taking a toxin away from the bacteria and analysing it has considerable merit,” he says, “but it only tells part of the story.”

C. difficile diagnosis, treatment and prevention now will need to focus on toxin B.”

What’s next for the dynamic duo? They plan to nail how pesky C. difficile spores lodge in the gut and block that process - and hopefully prevent infection - a challenge that they both relish.

“We work on bugs that other people think are too difficult to study, then crack their genetics and figure out how they cause disease,” Professor Rood says.

 
Dr Dena Lyras with Prof Julian Rood