*Malassezia sympodialis* May Help Stop Staph Infections

A lethal superbug responsible for the deaths of more than a million people worldwide each year may have an adversary living directly beneath your nose.

Quite literally: it is highly abundant in your skin microbiome, where it appears to hold staph infections in check.

Malassezia sympodialis and the skin microbiome

The largely overlooked defender is a naturally occurring yeast species named Malassezia sympodialis, among the most common microorganisms found on healthy human skin. As it breaks down oil and fat on the surface of the body, this fungus can generate a fatty acid that prevents a staph infection from developing and growing, new research indicates.

Laboratory experiments led by researchers at the University of Oregon (UO) show that M. sympodialis can act against Staphylococcus aureus bacteria via its acidic byproducts.

The acid made by the yeast is frequently found on healthy skin, leading researchers to believe it prevents S. aureus from excessively colonising the microbiome. Although S. aureus normally forms part of the skin microbiome, it can cause serious infections when it becomes dominant or enters tissue or the bloodstream.

Why staph infections remain a serious threat

Skin and soft-tissue infections involving S. aureus lead to roughly 500,000 hospitalisations each year in the United States. The bacterium can also develop resistance to every class of antibiotics currently available.

As a result, new drug treatments must continually be developed to keep pace with its deadly impact. The skin microbiome's own natural protection against staph infections therefore warrants further investigation.

"There are lots of studies that identify new antibiotic structures," says lead author and evolutionary biologist Caitlin Kowalski from UO, "but what was fun and interesting about ours is that we identified (a compound) that is well-known and that people have studied before."

That compound is 10-hydroxy palmitic acid (10-HP). Scientists may have previously missed its antimicrobial properties because it releases its toxic effects only in a low-pH setting, such as the skin, rather than under standard laboratory conditions.

Using skin biopsy samples from healthy human donors, Kowalski and her colleagues determined that resident Malassezia yeast produced the acid.

"It was like finding a needle in a haystack but with molecules you can't see," says Kowalski's adviser, biologist Matthew Barber.

Testing 10-HP against S. aureus

Barber, Kowalski and their colleagues tested in the laboratory how M. sympodialis yeast affected several strains of S. aureus. Following two hours of yeast treatment, most S. aureus strains experienced a greater than 100-fold drop in viability.

With time, S. aureus strains gained a degree of resistance to M. sympodialis' 10-HP. The harmful bacteria achieved this in a way similar to their development of tolerance to clinical antibiotics.

The researchers also found that other Staphylococcus species, which are not as dangerous as S. aureus, had already developed comparable means of living alongside M. sympodialis yeast.

"Given the prevalence of Malassezia within the mammalian skin microbiota, we are likely just scratching the surface of its roles in shaping microbial interactions and colonization resistance in this niche," write the authors.

Kowalski now intends to examine the genetic mechanisms behind antibiotic-resistant staph infections in depth, to gain a clearer understanding of how the bacteria mutate so quickly to evade a broad range of antimicrobial agents.

"We still have a lot of work to do in understanding the microorganisms, and also finding new ways that we can possibly treat or prevent those infections," says Barber.

The study was published in Current Biology.