Researchers fight resistant bugs

Researchers at the University of North Carolina at Chapel Hill have discovered that two drugs used to treat bone loss in old folks can both kill and short-circuit the “sex life” of antibiotic-resistant bacteria blamed for nearly 100,000 hospital deaths across the country each year.

Unveiled Monday and slated for publication in a scientific journal this week, the UNC research breakthrough holds the promise of opening a new avenue of attack against bacteria that have become increasingly resistant to existing antibiotics and often take a shorter time to develop this invulnerability and pass it along to other bugs, said Matt Redinbo, senior author of the new study.

“Potentially, we have a brand new way to kill the most dangerous bacteria that are out there,” said Redinbo, a UNC professor of chemistry, biochemistry and biophysics. “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 U.S. alone, the Centers for Disease Control and Prevention estimate 1.7 million hospital patients get an infection each year, while 99,000 of those patients die. 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 second- or third-choice medicine that may be less effective, more toxic and more expensive. These treatments drive 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, from isolation of infected patients to requiring the use of masks, gloves and other protective gear for doctors and nurses.

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 and medical academics, while cautious not to over-hype these early results, are hoping for a bigger payoff from the laboratory discovery of one of Redinbo’s graduate students, Scott Lujan.

So far, UNC laboratory research on E. coli bacteria brought a hoped-for result — the 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 for fuller scientific proof, also produced a surprise — the two drugs killed any bug that already had the antibiotic-resistant gene.

“We didn’t expect this,” said Redinbo, whose study will be published online this week 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,” much like a plug-in for a computer software program.

The bugs not only pass this information between the same strain of bacteria but between different strains of bacteria, increasing the problem of antibiotic resistance, said Dr. David Hecht, professor of medicine, microbiology and immunology and infectious disease division chief at Loyala University Health Systems near Chicago.

Most antibiotics attack infectious bugs by breaking down the cell wall that holds bacteria together or knocking out the “protein factory” necessary for growth and survival. But if Lujan's discovery works on other stubborn bacteria, the long-term result could be a new family of antibiotics based on a type of drug already approved for use in humans.

That would save pharmaceutical companies the massive research and development costs of bringing a brand new drug to market, said Scott Singleton, a professor in UNC’s School of Pharmacy who has also been studying the problem of antibiotic-resistant bacteria.

“I think it’s huge,” Singleton said of Redinbo and Lujan’s research. “It’s a dramatic shortcut.”

News researcher Denise Jones contributed to this report.