These bacteria keep swapping resistance genes, even with no antibiotics around

The growing threat of antibiotic resistance has sparked calls to use antibiotics more responsibly to curb the spread of drug-resistant bacteria. The idea: If we reduce antibiotic use, we could reduce the resistance that’s been naturally selected for over time.

But new research published Wednesday in Nature Communications finds that isn’t always the case.

STAT chatted with biomedical researcher Allison Lopatkin of Duke about the discovery.

How did you study the spread of antibiotic resistance between bacteria?

We looked at something called horizontal gene transfer, the primary way that new bacteria acquire antibiotic resistance genes. One of the main methods is gene transfer is called conjugation. It’s literally just two cells that knock into one another and one transfers the DNA. This DNA is often located in these really transferable elements called plasmids. We looked at if we totally remove antibiotics, will the resistance gene on these plasmids disappear? If there’s an antibiotic present, the cell with the plasmid grows better because it can resist the antibiotic. But without antibiotics present, cells without plasmid often reproduce faster, because there’s less of a burden on them. Will bacteria take advantage of that fact?

What did you see happening?

What we saw is the plasmids are transferable through this process of conjugation and even though those cells are growing slower, the resistance doesn’t go anywhere. The plasmid can be transferred so fast that even for really, really costly plasmids, we can remove antibiotics entirely and the resistance will still exist. It’s continuously infecting new cells. That’s a really concerning conclusion.

But you found a potential way to intervene.

We looked at what happened when we combined two compounds, one which inhibits gene transfer and one which promotes the rate of plasmid loss. That compound makes it much more likely there’s no plasmid on the daughter cells when a cell divides. We were able to reverse resistance four out of the nine plasmids we studied, and we could prevent the spread resistance in the remaining five.