Scientists Explore the Mechanism of Antibiotic Resistance in Bacteria

It has long been understood that incomplete antibiotic treatment can lead to the formation of drug-resistant bacteria. Researchers in a new study have set out to explore the exact mechanism by which this happens.


The Resurgence of Antibiotic-resistant Bacteria

When someone begins on antibiotic treatment, most of the bacteria are killed off. Some remaining bacteria, which are nearly dead, can recover. This is the beginning of resistance. The study by Christian Lesterlin, a bacterial geneticist of CNRS-INSERM and colleagues at the University of Lyon in France reveals how the harmful bacteria can make a comeback. The findings were recently published in Science.

The team found that a protein known as AcrAB-TolC multidrug efflux pump was behind the survival of E. coli bacteria treated with an antibiotic. This protein can pump toxic chemicals out of the bacterial cells, which delays their effects and gives time for the bacteria to become drug-resistant. The protein pump cannot counter antibiotics itself, but its ability to keep affected bacteria alive for longer gives an opportunity for surviving cells to start producing drug-resistant proteins.

Antibiotic-resistant bacterial cells give rise to more antibiotic-resistant cells. This propagation of resistance is a challenge for the health industry that has affected the treatment and recovery of many, many affected people. Anti-biotic resistant bacteria carry the genes for this important capability in rings of DNA known as plasmids. Bacteria can swap these plasmids between each other, and this leads to an exchange of DNA material and passes antibiotic-resistance to another bacteria.

This mechanism of gene swapping has long been known, but it was believed that this happened when there were no more antibiotics to kill off the sensitive bacteria. The new research used E.coli bacteria modified with fluorescent proteins to allow scientists to watch the plasmid swapping using a microscope. This revealed that the swaps happen very quickly both in the presence and absence of the antibiotic.

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