If you want to see evolution at work, visit a hospital. Inside a sick patient, antibiotics wipe out infectious bacteria by the millions. But germs are always mutating. A few adapt to resist the drug, so they survive—and spread. Such antibiotic-resistant bacteria infect two million Americans every year; they kill 23,000. In this arms race between medicine and evolution, evolution is winning.
But could we turn evolution against bacteria?
It turns out that when bacteria mutate to become resistant to one antibiotic, they often become more vulnerable to a different drug. So maybe after a jab with the left, a roundhouse to the right will deliver a knockout blow.
To test this idea, researchers in Denmark dosed batches of E. coli with 23 different antibiotics, and waited for resistance to evolve. In three-quarters of the cases, the mutant germs became more susceptible to a second drug.
The work appears in the journal Science Translational Medicine. [Lejla Imamovic and Morten O. A. Sommer, Use of Collateral Sensitivity Networks to Design Drug Cycling Protocols That Avoid Resistance Development]
One particular combination of widely used antibiotics—gentamicin, then cefuroxime, then gentamicin again, and so on—looks like it could hold the bugs at bay indefinitely.
[The above text is a transcript of this podcast.]