Scientists say it might be possible to stop drug-resistant superbugs without developing new antibiotics.
When bacteria strike to kill other bacteria, they turn off their antibiotic-resistance genes, leaving them vulnerable to antibiotics.
“If we can identify ways to force the entire population of drug-resistant bacteria to undergo this change, we stand a better chance of fighting the growing problem of antibiotic resistance,” says Brent Weber, a graduate student at Washington University School of Medicine in St. Louis. “Instead of looking for new antibiotics, we could restore bacteria’s vulnerability to antibiotics we already have.”
The researchers studied samples of multidrug-resistant Acinetobacter baumannii, a frequent cause of difficult-to-treat infections in hospitals, isolated from a 2012 outbreak at a Canadian hospital. Four patients were infected, and one died.
“Many strains of this type of bacteria are resistant to antibiotics, can survive disinfectants and rapidly are becoming major health problems in hospitals worldwide,” says Mario Feldman, associate professor of molecular microbiology and senior author of the study published in the Proceedings of the National Academy of Sciences.
The researchers expected the bacteria to readily kill other bacteria by producing and injecting a poison into their bacterial competitors. Killing the competitors should help A. baumannii infections spread widely and quickly.
But instead, the scientists found that the bacteria’s poison injection system was disabled in most of the samples from the Canadian outbreak. They identified chunks of bacterial DNA that were shutting down the system. These pieces of DNA, known as plasmids, also carried genes that enabled the bacteria to resist antibiotics.
In addition, the scientists found that part of the bacterial population regularly deactivated the plasmids, which turned on the poison injection system and transformed the bacteria into killers. But doing so meant the bacteria also turned off the antibiotic-resistance genes.
Additional studies of A. baumannii samples from other outbreaks worldwide found the same trade-off: the bacteria’s ability to kill competitors could be activated but doing so left them at the mercy of antibiotics.
“This appears to be a common strategy for these bacteria in different parts of the world, and further study could help us understand how bacteria evolve into superbugs that are resistant to many forms of treatment,” Feldman says. “This knowledge could lead to more effective treatments and better strategies for preventing the development of superbugs.”
The National Sciences and Engineering Research Council of Canada funded the study.