Analysis of Colonization and Genotyping of the Exotoxins of Staphylococcus aureus in Patients with Atopic Dermatitis

BACKGROUND: The skin of atopic dermatitis (AD) patients has a high susceptibility to Staphylococcus aureus colonization, and the toxins produced by S. aureus may aggravate AD by acting as superantigens. OBJECTIVE: The purpose of this study was to evaluate the relationship of the skin barrier function, colonization of S. aureus, and the clinical severity of AD. We also examined the predominant toxin genes produced in Korean AD patients. METHODS: Thirty-nine patients with AD were evaluated for clinical severity and skin barrier function by using Severity Scoring of Atopic Dermatitis (SCORAD) index and transepidermal water loss (TEWL). S. aureus was isolated from the forearm, popliteal fossa, and anterior nares of AD patients (n=39) and age-matched controls (n=40); the toxin genes were analyzed by performing multiplex polymerase chain reaction. RESULTS: TEWL showed a statistically significant correlation with clinical severity in patients with AD (p<0.05). TEWL was correlated with the number of S. aureus colonization sites and the presence of nasal colonization, but these results were not statistically significant. S. aureus strains were isolated in 64.1% of the 39 AD patients. The SCORAD index and AD severity were strongly correlated with the number of colonization sites. The predominant toxin gene found in AD patients was staphylococcal enterotoxin a (sea) only, which was produced in 52.6% of patients. The toxin genes sea and toxic shock syndrome toxin-1 (tsst-1) were found together in 42.1%, while tsst-1 only was found in 5.3% of the patients. CONCLUSION: S. aureus strains were isolated in 64.1% of the 39 AD patients. Skin barrier function, as measured by TEWL, revealed a statistically significant correlation with clinical severity in AD patients. The SCORAD index and severity of AD was strongly correlated with the number of colonization. The most common toxin gene was sea in the Korean AD patients and this gene might have an important role in the pathogenesis of AD.