By Nicole Loranger
Current research from the University of San Diego Medical School has provided new insight and breakthrough treatment for a common but serious skin infection. This condition, the most prevalent form of eczema known as atopic dermatitis, plagues 18 million people in the United States alone, causing a painful rash on the arms, legs and cheeks. Knowing that the average, healthy human has millions of bacteria on their skin, these researchers from the UCSD Dermatology Department screened for antimicrobial properties amongst common epidermal bacteria- 10,000 colonies, to be exact. In doing so, the team discovered colonies that secrete peptides capable of targeting harmful bacteria, an interaction that occurs successfully on healthy human skin but appears to to be lacking on the skin of patients with atopic dermatitis. By defending the skin against the harmful bacteria, S. aureus, benevolent bacterial strains such as S. hominis and S. epidermis are also helping to prevent the development of MRSA, the methicillin-resistant form of S. aureus and leading cause of death by infection in the U.S. Understanding the important role these “good” bacteria play, the researchers tested the effects of a bacterial transplant, a trial that saw overwhelming success. According to Dr. Richard Gallo, head of the Dermatology Department, the transplant was initially only intended to test for safety and efficacy, but saw an “immediate impact by reducing the amount of S. aureus on [infected patients’] skin.” Because this treatment utilizes bacteria already found on the skin, it will not wipe out colonies of these “good bacteria”, targeting only the pathogenic strains behind the infection. For this reason, it will not likely result in antibiotic resistance overtime- demonstrating the great deal of promise this study has in the fight against infection.
University of California San Diego Health Sciences. "Transplanting good bacteria to kill staph." ScienceDaily. ScienceDaily, 22 February 2017. <www.sciencedaily.com/releases/2017/02/170222150302.htm>.