It’s estimated the skin condition eczema afflicts some 18 million Americans. Ezcmea is actually a category of skin irritations, the most common of which is atopic dermatitis (AD). “Atopic” means “hereditary,” by the way. In any event, the stuff itches at best, and can result in serious irritations and cracked and oozing skin at worst. (Sorry, were you eating?). It’s also difficult to get under control. Now a study suggests that it may be possible to prevent AD, or even treat it, using beneficial bacteria already on your own skin.
As we’ve come to understand our microbiomes , we’ve realized there’s good bacteria — from our point of view, of course — and bad. Staphylococcus aureus would be one of the latter kind, and it’s known to aggravate AD. (We don’t yet know if it causes it.) Staphylococcus aureus is known as “Golden staph” and is also a precursor to MRSA, the antibiotic-resistant superbug.
Golden staph (NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASE)
Knowing that everyone’s skin hosts various types of bacteria, Richard Gallo, dermatology chairman at the University of California, San Diego, wanted to have a closer look at why some people have issues with AD while others don’t. He and his team took swabs from 49 people with AD and 30 people with healthy skin.
What they found was that those with healthy skin had greater numbers of two beneficial bacteria called Staphylococcus hominis and Staphylococcus epidermis. These bacteria are known to secrete “antibacterial peptides” that act as natural antibiotics shown in lab cultures and on animal skin to kill Staphylococcus aureus, and even a strain of MRSA, without harming other bacteria. (Man-made antibiotics are blunt instruments that kill off beneficial bacteria at the same time as they attack harmful strains.) As it turns out, there was less of these good bacteria on the skin of people with AD. Gallo told the Associated Press, “People with this type of eczema, for some reason that’s not quite known yet, have a lot of bacteria on the skin but it’s the wrong type of bacteria. They’re not producing the antimicrobials they need.”
(ORRLING AND TOMER S)
The team identified five volunteers who had Staphylococcus aureus on their skin but hadn’t yet developed AD. They collected Staphylococcus hominis and Staphylococcus epidermis from each subject’s skin and mixed it together with some over-the-counter moisturizer. The subjects were then instructed to apply their personalized moisturizer on one arm and regular cream on the other. By the next day, with three of the five subjects, the tweaked moisturizer had killed off most of the Staphylococcus aureus; for the other two, it had eliminated it altogether. ““We’re encouraged that we see the Staph aureus, which we know makes the disease worse, go away,” Gallo said.
It’s still unknown whether a similar approach will help patients who’ve already developed AD, and what the approach’s long-term affects would be, but next-step clinical trials are underway.
More Staphylococcus aureus