Discovery May Lead to New Antibiotic

May 08, 2013 - News Release

Novel ways of treating bacterial diseases such as meningitis and some bloodstream infections may one day result from a new discovery by University of Guelph microbiologists.

Uncovering a key piece of bacterial machinery that helps pathogens don a surface coat to outwit the body’s natural immunity might give physicians a new way to treat microbes causing serious illness and even death, said Lisa Willis, a PhD student in the Department of Molecular and Cellular Biology (MCB).

“It would be a new kind of antibiotic,” said Willis, lead author of a new paper published online last month in the Proceedings of the National Academy of Sciences.

Her co-authors are her adviser -- MCB chair Prof. Chris Whitfield -- and scientists at the National Research Council of Canada and the University of Alberta.

Willis said the team’s discovery promises a way to disrupt the protective surface coat of virulent bacteria. That would allow the body’s immune system to remove the pathogen normally.

“The bacteria can survive fine without this virulence factor in the lab – they just can’t cause disease,” she said.

The researchers cautioned that it may take years to develop treatments. Said Whitfield, “This identifies a good target for therapeutics, but drug discovery is a long process, followed by clinical trials of any new antibiotic.”

Using viruses that attack bacteria, Willis isolated and identified a critical component on the surface of many bacterial cells. Those microbes include pathogens causing meningitis and infections of the bloodstream and urinary tract in people, as well as bacteria that cause various livestock diseases.

Because the molecule is found in bacteria but not in humans, drug companies might target treatments without harming human cells, said Willis.

The researchers looked at enzymes needed to make the cell surface component, which is part of a larger sugar molecule.

“Without these enzymes, the cell can’t make these complex sugars and can’t assemble the surface coat,” said Whitfield. “If you’re able to target the initial enzyme, you turn the entire process off.”

Finding such a crucial target may help combat drug-resistant bacteria, he said. “This step is essential for these bacteria to cause disease. There is no secondary route that we know of that might fill the gap.”

This research was funded by the Canadian Institutes of Health Research and the Natural Sciences and Engineering Research Council, and by Whitfield’s Canada Research Chair in Molecular Microbiology.

For media questions, contact Communications and Public Affairs: Lori Bona Hunt, 519-824-4120, Ext. 53338,; or Kevin Gonsalves, Ext. 56982,

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