Dr. Herbert B. Allen, a professor at the Drexel University College of Medicine and the chairman of the dermatology department, has reportedly discovered the cause of eczema, an inflammatory and itchy skin disorder. The report, released online Jan. 22 via JAMA Dermatology, states that the staphylococcal bacteria that live on the skin may be the cause of eczema. Such bacteria produce a biofilm that blocks sweat ducts, which activates molecules in the body’s immune system, causing itching and irritation.
About 30 million people in America have eczema, which is a collective term for disorders that result in inflamed, irritated skin. The most common of these disorders is atopic dermatitis, or AD. People with eczema are typically diagnosed when they are infants or young children, and it usually becomes less severe in adulthood.
Allen started his research four years ago because he was interested in finding out the cause of eczema rather than fighting the disease itself.
“We knew it was worse when people were sweating. I wondered if it might be similar to miliaria (prickly heat), where the sweat ducts become occluded and cause itching,” he said.
Dr. Suresh Joshi, a research assistant professor in the departments of Surgery and Microbiology & Immunology and the director of surgical site infection and bacterial pathogenesis, said they started their research by investigating many cases of eczema and isolated the variables of possible causes.
“When we found the bacterium, that’s where the research [really] started,” Joshi said.
During the course of the study, Allen and his colleagues obtained both lesion and non-lesion swabs from 40 patients with atopic dermatitis, as well as 20 samples from individuals without AD. He said that the bacteria related to the disease, Staphylococcus aureus, produces a biofilm for protection when it comes into contact with salt or water.
“It makes up 20 percent of bacteria on the skin, but 40 percent on lesions. Everybody has it,” Allen said.
This biofilm occludes the skin’s sweat ducts, which triggers a reaction in Toll-like receptor 2, one of the “first responders” of the immune system. However, eczema has both biological and environmental factors.
“The one other thing that is super important is this filaggrin gene deficiency,” Allen said. “If you have that deficiency, and you have occluded sweat ducts, you get the itching. If you don’t have the gene, you get prickly heat.”
It has been theorized in the scientific community for more than 20 years that Staphylococcus aureus is connected to eczema. When asked why further investigation into the matter had not been done before now, Allen responded by saying “People don’t study common diseases as much as uncommon diseases. They thought that finding the bacteria was the most important thing. Our finding out what it does is probably the most important thing in the paper.”
He also has some advice on countering eczema’s occurrence. “If you take care of [the outer layer of your] skin, you prevent reoccurrence. You use less soap, less hot water, more moisturizer,” he said.
The research team does have plans for continuing their research. “Mostly we will be looking at genetic and molecular expression, so this is just the beginning,” Joshi said.
“Just as related to biofilms, we’re going to be looking at [a type of fungal tissue], and the effects of different bacteria on [skin disease] and various permutations there,” Allen added.