Addressing the Microbiome in AD: What Dysbiosis Reveals About Infection Risk

Infection is among the most clinically consequential and underappreciated comorbidities in atopic dermatitis (AD), according to , Adam Friedman, MD, FAAD, who addressed the topic in a presentation at the Revolutionizing Atopic Dermatitis 2026 Conference in Nashville, Tennessee. The relationship, he explained, is bidirectional and begins well before a frank infection takes hold.

Friedman, professor and chair of dermatology at the George Washington University School of Medicine and Health Sciences, described the skin of AD patients as uniquely hospitable to pathogens. "There is something really unique with atopic dermatitis, where it's a love-hate relationship between pathogens and atopic dermatitis skin," he said in an interview with Dermatology Times.

The pH Problem: How AD Disrupts the Microbiome

Understanding the difference between healthy skin and atopic skin is important, Friedman explained. Healthy skin maintains an acidic pH that supports a diverse community of microorganisms of roughly 500 or more species. "In AD, at baseline, it's a basic pH, which messes with that diversity, but also fosters an environment that's great for staph aureus," Friedman said. The resulting dysbiosis is not a passive bystander. He referred to research from Heidi H. Kong, MD, MHSc, and colleagues and Elizabeth Bryce, MD, FRCPC, and colleagues that has shown that decreased microbial diversity actually precedes AD flares, suggesting the microbiome is an active driver of inflammation, not merely a casualty of it.

From Dysbiosis to Infection: Why the Armor Is Down

Dysbiosis, Friedman emphasized, is distinct from infection but it sets the stage. The immune milieu in AD suppresses the innate immune response, including antimicrobial peptides, which he described as "the ninjas, so to speak, of the immune system that literally chop up the pathogen trying to get through." Without these defenses, bacterial and viral pathogens face little resistance at the skin barrier.

The bacterial culprit most clinicians reach for is Staphylococcus aureus, Friedman told Dermatology Times, but there are others to consider. "In my talk here at RAD, I also mentioned strep. We cannot forget strep either, because strep is not going to be sensitive to all antibiotics we might think about when it comes to the management of bacterial infections."

Viral Threats: Herpeticum, Coccacum, and Molluscum

The infection risk in AD extends beyond bacteria. Friedman outlined 3 viral complications clinicians should keep on their radar. For example, eczema herpeticum, which is a potentially life-threatening superinfection with herpes simplex virus, carries heightened concern in pregnant patients, with implications for both mother and fetus. Eczema coxsackium, a robust cutaneous response to Coxsackie virus in the setting of hand, foot, and mouth disease, presents another concern. And while molluscum dermatitis often portends eventual clearance of molluscum contagiosum, the presence of AD independently increases a patient's susceptibility to molluscum infection.

The Bottom Line: Treat the AD, Treat the Infection

The most clinically actionable takeaway from Friedman's RAD 2026 presentation may be the simplest: in many cases, treating the AD is sufficient to resolve the infection without targeting the infection directly. Multiple studies examining both topical and systemic AD therapies have demonstrated infection improvement even when the infection itself goes untreated.

"You don't even have to treat the infection. You treat atopic dermatitis, the infection can actually improve just from that alone," Friedman told Dermatology Times. That finding reframes what's at stake when AD goes undertreated. "That really speaks to the harm of not treating, the side effect of not treating. Treating AD lessens that infection risk."

Additional conference coverage can be found here.