Antibiotic Resistance Crisis: Weakness Seen in Bacteria Killing Millions

The discovery of an "Achilles' heel" in strains of antibiotic-resistant bacteria may provide a better way to deal with this public health crisis. That is the conclusion of an international team of researchers from the University of California, San Diego (UCSD), which found that developing drug resistance comes with a drawback: It makes bacteria more dependent on magnesium to proliferate. "We are running out of effective antibiotics and their rampant use over the decades has resulted in antibiotics being spread across the globe, from the arctic to the oceans and our groundwater," UCSD molecular biologist and professor Gürol Süel said in a statement. "Drug-free alternatives to treating bacterial infections are needed—and our two most recent studies show how we can indeed achieve drug-free control over antibiotic resistant bacteria," he said.

Antibiotic resistance is a significant and escalating concern. It is estimated that more than 1 million people died from drug-resistant infections every year between 1990 and 2021. And this figure is expected to rise—with experts predicting it could reach a horrific 2 million deaths each year by the middle of the century. Accordingly, the scientific community is heavily invested in developing new antibiotics, along with promoting the use of existing ones only when needed to slow down the development of new drug-resistant bacterial strains. Another line of attack involves deciphering the mechanisms involved in both bacterial infection and the development of antibiotic-resistance genes.

In their study, Süel and his colleagues studied antibiotic resistance in the "hay bacillus" (Bacillus subtilis)—a bacterium found in both soil and the gastrointestinal tracts of humans, certain sponges and ruminant animals. The team wanted to know why bacteria that gain antibiotic resistance via spontaneous mutation do not go on to dominate the rest of their populations, seeing as they have an apparent major advantage. They focused on the bacteria's ribosomes, which are cellular micro-machines that are key to making proteins and translating genetic codes, and magnesium ions, which all cells rely on to survive. Analysis revealed that the ribosomes in antibiotic strains of hay bacillus require more magnesium than their regular counterparts—to the extent that they can end up competing for these ions with the so-called ATP molecules that provide energy to the bacterial cells, ultimately impeding the cells' growth. "While we often think of antibiotic resistance as a major benefit for bacteria to survive, we found that the ability to cope with magnesium limitation in their environment is more important for bacterial proliferation," Süel said. He continued: "We discovered an Achilles' heel of antibiotic resistant bacteria. We can take advantage of this cost to suppress the establishment of antibiotic resistance without drugs or harmful chemicals." One possible next step, the team said, is to see if it is possible to artificially limit the accessibility of magnesium in bacterial environments—basically starving the antibiotic bacteria without hurting the good bacteria that are essential to our health. Do you have a tip on a science story that Newsweek should be covering? Do you have a question about the microbes? Let us know via science@newsweek.com.

References

Moon, E. C., Modi, T., Lee, D.-Y. D., Yangaliev, D., Garcia-Ojalvo, J., Ozkan, S. B., & Süel, G. M. (2024). Physiological cost of antibiotic resistance: Insights from a ribosome variant in bacteria. Science Advances, 10. https://doi.org/10.1126/sciadv.adq5249 Naghavi, M., Vollset, S. E., Ikuta, K. S., Swetschinski, L. R., Gray, A. P., Wool, E. E., Aguilar, G. R., Mestrovic, T., Smith, G., Han, C., Hsu, R. L., Chalek, J., Araki, D. T., Chung, E., Raggi, C., Hayoon, A. G., Weaver, N. D., Lindstedt, P. A., Smith, A. E., ... Murray, C. J. L. (2024). Global burden of bacterial antimicrobial resistance 1990–2021: A systematic analysis with forecasts to 2050. The Lancet, 404(10459), 1199–1226. https://doi.org/10.1016/S0140-6736(24)01867-1