Superantigen Profile ofStaphylococcus aureusIsolates from Patients with Steroid‐Resistant Atopic Dermatitis (original) (raw)

2008, Clinical Infectious Diseases

Background. Superantigens induce skin inflammatory responses in atopic dermatitis, which is commonly associated with Staphylococcus aureus infection. T cells activated in vitro by superantigens become steroid resistant. The objective was to assess the superantigen profiles of S. aureus isolates from patients with steroid-resistant atopic dermatitis. Methods. We compared the superantigen-production capability of S. aureus isolates from 78 patients with steroid-resistant atopic dermatitis (group 1) with that of 30 vaginal isolates from healthy women (group 2) and 22 isolates from a general population of patients with atopic dermatitis (group 3). Polymerase chain reaction with primers for superantigens, combined with selected antibody testing, was used to analyze the presence of toxic shock syndrome toxin 1, staphylococcal enterotoxins, and enterotoxin-like superantigens. Results. S. aureus isolates from group 1 had a statistically significant difference in superantigen profile, compared with the profiles of group 2 and group 3 isolates. Group 2 isolates were similar in profile to group 3 isolates, with 4 and 5 superantigens per isolate, respectively. In contrast, group 1 isolates produced a mean of 8 superantigens each (, for comparison with group 2 or group 3). These group 1 isolates were more likely to produce the P K .001 3 major toxic shock syndrome-associated superantigens (toxic shock syndrome toxin 1, staphylococcal enterotoxin B, and staphylococcal enterotoxin C) and to produce unusual combinations of superantigens (e.g., toxic shock syndrome toxin 1 and staphylococcal enterotoxin B). Conclusions. S. aureus isolates from patients with steroid-resistant atopic dermatitis appear to be selected on the basis of greater production of superantigens, compared with that of isolates from control groups. Superantigens may offer selective advantages for colonization of patients. Staphylococcus aureus is a commensal organism that colonizes up to 50% of humans [1, 2]. The organism most often colonizes the anterior nares and, from there, may colonize other body surfaces, including other mucous membranes and damaged skin. S. aureus causes a wide variety of human illnesses, including scalded skin syndrome, toxic shock syndrome (TSS), and necrotizing pneumonia [3-9]. The ability of S. aureus to cause human disease depends on the production of cell-surface adhesins, an