Researchers at Washington University have found that some multidrug resistant bacteria intentionally get rid of the genes that protect them from antibiotics. That discovery could eventually provide a new way to treat deadly infections.
Molecular microbiologist Mario Feldman, who led the study, said that in the past, infections caused by a bacterium known as Asinetobacter baumannii were easily treated with antibiotics.
“We have some new strains that are resistant to all the antibiotics we have,” Feldman said.
Researchers began paying attention to A. baumannii when American soldiers started coming back from Iraq with drug-resistant infections. The superbug — nicknamed the “Iraqibacter” — spread to civilian hospitals, where it currently infects an estimated 7,300 patients each year — about 500 of whom don’t survive.
In all, more than 23,000 Americans die annually from infections caused by some kind of multidrug-resistant bacteria.
“We are officially in the post-antibiotic era,” Feldman said. “Bacteria — we thought that they were simple and stupid unicellular organisms. But they are showing us that they’re very smart and they can learn all the tricks on how to survive our antibiotics.”
Feldman said bacteria can quickly adapt to any new drug we deploy “much faster than normal evolution that we see in nature. We need to find new ways to fight against them.”
Feldman’s research team may have done just that.
His graduate student Brent Weber found that in order to kill other, competing bacteria, A. baumannii has to get rid of a piece of its own DNA — a piece called a plasmid — that otherwise suppresses its ability to attack.
That same plasmid carries the bacteria’s genes for antibiotic resistance.
“It seems like a pretty hefty trade-off,” Weber said. “All these antibiotic resistance genes that might have taken years and years to acquire, it just kicks them right out and becomes totally antibiotic sensitive. But it gains this ability to kill other bacteria.”
Weber said the ability for some bacterial cells to out-compete rival microbes, while others fend off antibiotics, likely helps A. baumannii maintain a growing population — and keeps us from recovering from infection.
But Feldman believes that in future, we could use A. baumannii’s genetic trade-off to our advantage. “If we could learn how to force bacteria to lose this plasmid, then they will all naturally lose the antibiotic resistance,” Feldman said. That would mean that instead of constantly having to try to develop new, stronger antibiotics, we could just use the ones we already have.
Any medical applications are still years away, but Feldman said to fight antibiotic resistance, we first need to understand how it works. “The best strategy is to know your enemy,” Feldman said. “And for this we need to understand how bacteria use different mechanisms to resist antibiotics.”
Feldman and Weber's research was supported by funding from the National Sciences and Engineering Research Council of Canada and is published in the Proceedings of the National Academy of Sciences.
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