New findings suggest Staphylococcus aureus bacteria has evolved to grow faster on the skin of people with the chronic skin condition atopic dermatitis, also known as eczema.
While S. aureus bacteria is mostly harmless in people with healthy skin, the inflammation and cracks in the skin of people with eczema allow the bacteria to colonize the inflamed areas and cause ongoing, chronic infections.
A research collaboration, led by MIT and the National Institute for Pediatrics, Mexico City, shows that S. aureus bacteria on the skin of people with eczema evolves to adapt to its environment, making it harder to treat.
“This is the first study to show that Staph aureus genotypes are changing on people with atopic dermatitis,” said Tami Lieberman, an assistant professor at MIT and co-lead researcher on the study, in a press statement. “To my knowledge, this is the most direct evidence of adaptive evolution in the skin microbiome.”
Writing in the journal Cell Host & Microbe, Lieberman and co-investigators explain that a particular mutation in the bacterial capsule synthesis gene capD is common in people with eczema. “The capD gene encodes an enzyme that performs the first step in synthesizing the capsular polysaccharide of S. aureus,” explain the authors.
“The polysaccharide capsule of S. aureus… is generally considered a virulence factor that shields the pathogen from phagocytosis and the innate immune system. However… it has been shown that capsule-negative S. aureus exhibits improved adherence to fibrinogen, platelets, and endothelial cells.”
In this study, Lieberman and colleagues first tracked changes in S. aureus bacteria in 23 children being treated for atopic dermatitis. They found that S. aureus mutates and adapts once it has colonized a person’s skin with certain variants becoming more common than others. The team noted that capD mutations had appeared and become common in the skin microbiome of around a quarter of the children.
They then analyzed the S. aureus genomes taken from the skin of 276 additional people with atopic dermatitis and found a similar number (22.5%) had CapD mutations versus only 7.2% of healthy controls.
“Our findings in this study provide clues as to how S. aureus is evolving inside hosts and reveal some of the features that might help the bacteria to stay on the skin and generate disease versus being able to be swiped off,” said Maria Teresa García-Romero, a dermatologist and assistant professor at the National Institute of Pediatrics in Mexico, as well as co-lead author on the study.
“In the future, S. aureus variants with mutations in the capsular polysaccharide could be a relevant target for potential treatments,” she concluded.