Potential Drug Shows Promise in Slowing Down Bacteria’s Evolution of Antibiotic Resistance

The widespread misuse of antibiotics has resulted in the emergence of antibiotic-resistant bacteria, leading to a global health crisis.

Antibiotics, once considered miraculous drugs, have lost their stature due to the rampant abuse by individuals. This abuse has spurred the development of bacterial antibiotic resistance, a burgeoning global health emergency responsible for causing at least 1.3 million deaths in 2019 alone.

The emergence of antibiotic resistance is driven by either the occurrence of new bacterial mutations or the acquisition of resistance genes from other bacteria.

A team of researchers recently published a groundbreaking report on a drug that effectively reduces the ability of bacteria to develop antibiotic resistance. The drug, tested in both laboratory cultures and live animal models, inhibits the activation of the stress response in a common gut bacterium called Escherichia coli (E. coli). Repairing DNA breaks in the bacterial DNA creates new mutations during the stress response, which result in antibiotic resistance. Blocking this stress response could potentially extend the effectiveness of antibiotics.

“While most bacterial infections are cured after completing antibiotic treatment, there are cases where people don’t recover because the bacteria have developed resistance to the antibiotic, rendering it ineffective in killing the bacteria,” said senior author Susan Rosenberg, the Ben F. Love Chair in Cancer Research and professor at Baylor University.

For the study, Professor Rosenberg and her colleagues screened 1,120 drugs approved for human use to identify one that could impede or delay the evolution of antibiotic resistance in E. coli when the bacteria were exposed to the antibiotic ciprofloxacin (cipro). Previous research had revealed that stress responses in bacteria are triggered by low concentrations of cipro at the beginning and end of antibiotic treatment courses or when doses are missed.

The drug dequalinium chloride (DEQ) was identified through experimental screenings. Not only does DEQ reduce the ability of bacteria to develop antibiotic resistance, but it is also not an antibiotic itself, making it less likely that bacteria will acquire resistance to it.

“DEQ met both criteria,” said lead author Yin Zhai, a postdoctoral associate in the Rosenberg lab. “When combined with cipro, DEQ reduced the development of mutations that confer antibiotic resistance in laboratory cultures and animal models of infection. Furthermore, bacteria did not develop resistance to DEQ itself.”

This discovery is highly encouraging as many antibiotics become ineffective shortly after they become available, even for infections that have never been exposed to these new antibiotics before.

“Additionally, we achieved this beneficial effect at low DEQ concentrations, which bodes well for patients. Future clinical trials are required to assess the ability of DEQ to slow down bacterial antibiotic resistance in patients,” added Zhai.

Source:

Yin Zhai, John P. Pribis, SeanW. Dooling, Libertad Garcia-Villada, P.J. Minnick, Jun Xia, Jingjing Liu, Qian Mei, Devon M. Fitzgerald, Christophe Herman, P.J. Hastings, Mauro Costa-Mattioli and Susan M. Rosenberg (2023). Drugging evolution of antibiotic resistance at a regulatory network hub, Science Advances, 9(25) | doi:10.1126/sciadv.adg0188

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