We’ve written several stories stories over the years asking farmers to stop feeding unnecessary antibiotics to their animals, but it’s not because we object to the taste of penicillin. It’s because study after study has shown that the over-use of antibiotics contributes to the development of so-called superbugs, bacteria that are resistant to the very drugs intended to kill them. But researchers in Canada may have found a way to reverse that resistance.

The Wall Street Journal reports on research from scientists at McMaster University in Ontario who believe a compound, aspergillomarasmine A, extracted from a common fungus may hold the key to turning off drug resistance in bacteria.

According to the researchers, the compound has been shown to turn off the gene for an enzyme — New Delhi Metallo-beta-Lactamase-1, or NDM-1 — that gives bacteria the ability to survive antibiotic treatments.

When combining a purified form of the compound with an antibiotic, the researchers were able to deactivate the gene for NDM-1 in three drug-resistant superbugs. It removes zinc from the enzyme, which apparently makes the bacteria vulnerable to drugs again.

They tested on mice who had been injected with a lethal dose of drug-resistant bacteria. The compound on its own didn’t work, nor did the antibiotic. But when administered together, more than 95% of the mice survived.

In the U.S. alone, more than 2 million people every year become ill from drug-resistant microbes, with some 23,000 dying. If researchers can figure out exactly how much of the compound is needed to deactivate this gene and how to safely provide it to patients, that could help keep superbugs at bay, or at least give them something new to work on.

“Discovery of a fungus capable of rendering these multidrug-resistant organisms incapable of further infection is huge,” Irena Kenneley, a microbiologist and infectious disease specialist at Frances Payne Bolton School of Nursing at Case Western Reserve University, tells the Journal. “The availability of more treatment options will ultimately save many more lives.”

Of course, it will take a number of years and a lot more research and trials before any product reaches the market. And even then, there’s nothing to say that bacteria won’t just eventually develop a work-around that makes them resistant to the compound.

“I can’t imagine anything we could make where resistance would never be an issue,” admits the study’s lead researcher Gerard Wright, director of McMaster’s Michael G. DeGroote Institute for Infectious Disease Research. “At the end of the day, this is evolution and you can’t fight evolution.”

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