Two drugs used to treat bone loss in old age may provide a new weapon against antibiotic-resistant bacteria blamed for nearly 100,000 hospital deaths across the country each year, researchers at UNC-Chapel Hill discovered.

The drugs both snuff out hard-to-kill bacteria and short-circuit their "sex life," opening a possible new avenue of attack against bugs that have become increasingly resistant to common antibiotics, said Matt Redinbo, a UNC-CH professor of chemistry, biochemistry and biophysics.

"Potentially, we have a brand new way to kill the most dangerous bacteria that are out there," said Redinbo, senior author of the study released Monday and slated for online publication in a scientific journal this week. "It's becoming harder and harder to find drugs that effectively kill bacteria in humans."

From pneumonia and tuberculosis to simple staph infections, stubborn bacteria pose a dangerous worldwide medical threat from infectious diseases once thought conquered by miracle drugs such as penicillin or its pharmaceutical offspring. In the United States alone, the Centers for Disease Control and Prevention estimates 1.7 million hospital patients get an infection each year, with 99,000 dying. More than 70 percent of the bacteria that cause hospital infections are resistant to at least one of the antibiotics commonly used to treat them.

As a result, patients infected with resistant bacteria have longer hospital stays and require treatment with different medicines that may be more toxic and expensive, driving up health care costs, according to a CDC report. Hospitals have also been forced to develop expensive and cumbersome protocols to combat the spread of hard-to-kill bacteria, isolating infected patients and requiring doctors and nurses to wear masks, gloves and other protective gear.

Triangle hospital officials say they are caught in a squeeze play: More patients with stubborn infections; fewer antibiotics that are fully effective.

"The problem it creates for us in a hospital is that patients are sicker and harder to treat," said Robin Carver, interim director for infection prevention and control at WakeMed's main Raleigh campus. "Our options keep getting smaller and smaller and smaller."

That's why researchers, while cautious not to hype the early results, are hoping for a bigger payoff from the laboratory discovery of one of Redinbo's graduate students, Scott Lujan.

"The potential for its impact is great, but more research needs to be done," said Dr. David Hecht, professor of medicine, microbiology and immunology and infectious disease division chief at Loyola University Health Systems near Chicago.

Surprise in the lab

So far, UNC-CH laboratory research on E. coli bacteria brought a hoped-for result. Two off-the-shelf bone loss drugs, clodronate and etidronate, blocked a key mechanism used to squirt genetic changes from one bad bug into another, including the gene that helps ward off an antibiotic attack.

But the research, which still has to be duplicated in animals and humans, also produced a surprise -- the two drugs killed any bug that already had the antibiotic-resistant gene. The scientists aren't sure why this happened.

"We didn't expect this," said Redinbo, whose study will appear in the Proceedings of the National Academy of Sciences. "It kills the bad guys with the gun whether they're shooting it or not."

This discovery is important because a broad range of bacteria use this mechanism to pass along "genetic upgrades." The bugs not only pass this information between the same type of bacteria, but between different kinds of bacteria, exponentially increasing the problem of antibiotic resistance, Hecht said.

Next page >