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Study finds new genetic mutations behind antibiotic resistance

Researchers have uncovered new genetic mutations responsible for high-level antibiotic resistance.

By
Amy Wallace
New study has uncovered novel genetic mutations responsible for the development of antibiotic resistance. Photo by aterynaon/Shutterstock
New study has uncovered novel genetic mutations responsible for the development of antibiotic resistance. Photo by aterynaon/Shutterstock

Feb. 21 (UPI) -- Scientists from the Broad Institute of MIT and Harvard in Massachusetts, have identified new genetic mutations that cause high-level antibiotic resistance.

According to a 2013 report from the Centers for Disease Control and Prevention, antibiotic-resistant infections kill at least 23,000 people in the United States annually.

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"Some species of bacteria, including mycobacteria, develop drug resistance as a result of mutations in their genes," Deborah Hung, Core Institute Member, co-director of the Infectious Disease and Microbiome Program at the Broad Institute and senior author of the study, said in a press release. "We wanted to gain new insight into the molecular processes that promote resistance in these species by looking at the relationships between the concentration of antibiotics, their killing effects on bacteria, and the emergence of drug-resistant mutants."

Researchers grew hundreds of cultures of Mycobacterium smegmatis, related to the bacterium that causes tuberculosis. The bacteria was exposed to low antibiotic concentrations, where the drugs' microbe-killing effects were slow. The team then monitored the killing of sensitive bacteria while isolating individual wells where mutants developed.

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"We detected the outgrowth of drug-resistant mutants in a fraction of our cultures," James Gomez, first author of the study, said in a press release. "Each individual carried single mutations in different components of the ribosome, the complex molecular machine responsible for building proteins within cells."

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The study showed that ribosomal mutations gave the bacteria resistance to many different classes of antibiotics that do not target ribosome. The ribosomal mutations also increased resistance to heat shock and membrane stress.

"We did see a fitness cost to the bacteria in that the mutations reduced their growth rate," Gomez said. "However, the reprogramming that occurred within the cells in response to the mutations made the bacteria much less sensitive to both antibiotic and non-antibiotic stresses. This suggests that, in species such as M. smegmatis, these types of mutations can enhance fitness in multidrug environments and serve as stepping stones toward the development of high-level drug resistance, despite the cost that the mutations have on growth."

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The study was published in eLife.

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