Around 30 percent of people have Staphylococcus aureus bacteria — the primary bacterial culprit behind staphylococcal infections — somewhere on their skin or in their nose. In most cases, these spherically shaped bacteria stay out of trouble. But that’s only in most cases.
When presented with open wounds, scrapes, and scratches, S. aureus can invade and infect the body, and with serious consequences. In the skin, staph infections can cause boils, blisters, and inflammation. In the blood, they can cause septicemia and sepsis. And once there, they’re poised to travel to other places, too — to the lungs, to the heart, and to other internal organs, where they can create all sorts of problems.
It turns out, however, that scientists don’t have to look very far to find a solution for troublemaking S. aureus bacteria, which are famous for their resistance to clinical antibiotics. According to a new study in Current Biology, a team led by University of Oregon biologist Caitlin Kowalski has discovered a new antibiotic molecule that can successfully target S. aureus, at least for now. And the strangest thing is that it’s made by a fungus that’s also found on human skin.
Read More: Antibiotic-Resistant Bacteria: What They Are and How Scientists Are Combating Them
Fungi and the Skin Microbiome
Malassezia are a type of microscopic fungi that thrive on human skin, feeding on the ample lipids — the oils and the fats — that are found there and turning them into smaller fatty acids. These fungi are sometimes tied to the development of dandruff and other skin conditions, but mainly, they’re considered an abundant and mostly harmless member of the human skin microbiome, albeit a surprisingly understudied one.
“The skin is a parallel system to what’s happening in the gut, which is really well-studied,” Kowalski said in the release. “We know that the intestinal microbiome can modify host compounds and make their own unique compounds that have new functions. Skin is lipid-rich, and the skin microbiome processes these lipids to also produce bioactive compounds. So what does this mean for skin health and diseases?”
Hoping to learn more about the role of Malassezia in human health, Kowalski and her team studied skin samples in the lab and found that one species of Malassezia — M. sympodialis — transformed human skin lipids into smaller fatty acid molecules that attack S. aureus bacteria. According to the team, the molecules made by M. sympodialis and other fungi thus represent a new, and underutilized, resource in the fight against antibiotic-resistant bacteria.
Read More: Why Bacteria Are the New Disease Fighters
A For-Now Fix for Antibiotic Resistance
Though there are many studies out there that introduce potential solutions to the problem of antibiotic resistance, “what was fun and interesting about ours is that we identified (a compound) that is well-known and that people have studied before,” Kowalski said in the release.
Indeed, though the M. sympodialis molecules are a subject of prior research, their staph-stomping abilities are not. That may be because these molecules are only active against S. aureus on the skin — a surprisingly acidic surface — or in a lab setting meant to mimic the skin’s acidity.
“I think that’s why in some cases we may have missed these kinds of antimicrobial mechanisms,” Kowalski said in the release, “because the pH in the lab wasn’t low enough. But human skin is really acidic.”
In those skin-like lab conditions, the team found that the M. sympodialis molecules destroy the cellular membranes and drain the cellular contents of S. aureus bacteria mercilessly. Sapping the bacteria in only 15 minutes, the molecules are actually capable of stopping S. aureus colonization on the skin.
Though the M. sympodialis molecules represent one possible route for addressing the antibiotic resistance of S. aureus, they aren’t a permanent solution. In fact, the team found that S. aureus bacteria eventually evolve a tolerance against the molecules, in the same way that they eventually evolve a tolerance against clinical antibiotics. Emerging through a mutation in the Rel stress response gene, this tolerance is similar to the other tolerances that are seen in staph infection patients.
Evolution of Resistance
Taken together, the findings suggest that M. sympodialis antibiotics might work against staph, though they may not work forever.
“There’s growing interest in applying microbes as a therapeutic,” Kowalski said in the release. “But it can have consequences that we have not yet fully understood. Even though we know antibiotics lead to the evolution of resistance, it hasn’t been considered when we think about the application of microbes as a therapeutic.”
Still, Kowalski is eager to learn more. She said she has plans to continue to study the skin microbiome as a future source for antibiotics, and she’s even started a follow-up study to further test the tolerance of S. aureus to M. sympodialis molecules. The results might change the way we treat antibiotic-resistant bacteria, though they’re certain to change one thing: the way we think about our skin.
This article is not offering medical advice and should be used for informational purposes only.
Read More: Particularly Resilient Bacteria Are the Reason Why Antibiotics Can Fail
Article Sources
Our writers at Discovermagazine.com use peer-reviewed studies and high-quality sources for our articles, and our editors review for scientific accuracy and editorial standards. Review the sources used below for this article:
Cleveland Clinic. Staph Infection
Current Biology. Skin Mycobiota-Mediated Antagonism Against Staphylococcus Aureus Through a Modified Fatty Acid
Sam Walters is a journalist covering archaeology, paleontology, ecology, and evolution for Discover, along with an assortment of other topics. Before joining the Discover team as an assistant editor in 2022, Sam studied journalism at Northwestern University in Evanston, Illinois.
