Staphylococcus aureus bacteria are a major cause of serious infections that often persist despite antibiotic treatment.
In a recent study from the UNC School of Medicine, researchers have found a way to make these bacteria much more susceptible to some common antibiotics.
The study is published in Cell Chemical Biology. The lead author is Brian Conlon, Ph.D., an assistant professor in the department of microbiology and immunology at the UNC School of Medicine.
The U.S. Centers for Disease Control has estimated that in 2017 there were more than 119,000 cases of serious bloodstream Staph infections in the United States, of which more than 20,000 were fatal.
Standard treatments for many strains of the S. aureus do not kill the bacteria, either because the bacteria have genetically acquired specific antibiotic resistance or because they grow in the body in a way that makes them inherently less vulnerable.
There’s a great need for new ways to kill bacteria that tolerate or resist standard antibiotics.
In the study, the team found that adding molecules called rhamnolipids can make aminoglycoside antibiotics, such as tobramycin, hundreds of times more potent against S. aureus – including the strains that are otherwise very hard to kill.
Rhamnolipids are small molecules produced by another bacterial species.
The team also found rhamnolipid-tobramycin combinations could fight against S. aureus that is particularly hard to kill in ordinary clinical practice.
Moreover, the experiments showed that this potency-boosting strategy is effective not just against S. aureus but several other bacterial species that cause serious, often-fatal diarrheal illness among the elderly and patients in hospitals.
The team says there’s a huge number of bacterial interspecies interactions that could be influencing how well the antibiotics work.
They aim to improve the efficacy of current therapeutics and slowing the rise of antibiotic resistance.
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