This study is the first to directly observe such rapid evolution in a microbe associated with a complex skin disorder. The findings have potential implications for developing treatments that could target S. aureus variants with capD mutations to alleviate eczema symptoms, as these variants tend to exacerbate the condition.
The study, which was published in the scientific journal Cell Host and Microbe on April 12. The lead author of the paper is Felix Key, a former MIT postdoc who is now a group leader at the Max Planck Institute for Infection Biology. S. aureus is a common bacterium that is present in the nostrils of 30 to 60 percent of people and is usually harmless. However, in individuals with eczema, which affects millions of children and adults in the United States, S. aureus often spreads to eczema patches on the skin and causes infection.
The researchers in the study aimed to investigate how S. aureus is able to adapt to living on the skin of eczema patients. They recruited patients aged 5 to 15 who were being treated for moderate to severe eczema and collected samples of microbes from their skin once a month for three months, and then again at nine months. The samples were taken from various sites on the body, including the affected areas behind the knees and inside the elbows, as well as unaffected areas on the forearms and the nostrils.
The researchers cultured S. aureus cells from each sample site separately and sequenced their genomes once large colonies formed. This resulted in nearly 1500 unique colonies, allowing the researchers to closely observe the evolution of the bacterial cells in detail. They found that although most patients maintained a single lineage of S. aureus, a significant amount of mutation and evolution occurred within each lineage during the nine-month study period.
Interestingly, many of these mutations occurred in the capD gene, which codes for an enzyme involved in synthesizing the capsular polysaccharide, a protective coating that helps S. aureus evade recognition by immune cells. In two out of six patients with deep sampling, S. aureus strains with capD mutations became dominant in the entire population of S. aureus on the skin. In other patients, strains initially lacking a functional capD gene were also found, and by the end of the study, 22 percent of patients had S. aureus lacking capD. In one patient, multiple capD mutations arose independently in different S. aureus samples, and eventually, one variant became dominant and spread throughout the entire microbiome.
Further experiments in the lab showed that S. aureus strains with capD mutations grew faster than those with a normal capD gene. The researchers hypothesise that synthesizing the capsular polysaccharide requires a lot of energy, so when the cells do not have to produce it, they have more resources available for their own growth.
