Patients with atopic dermatitis (AD) are frequently colonized with Staphylococcus aureus (S.a) strains that secret exotoxins such as Staphylococcus enterotoxins enterotoxins A, B, C , D, E and Toxic shock syndrome toxin (SEA, SEB, SEC, SED, SEE and TSST), where SEA and SEB seem to be the most important ones involved in the IgE synthesis.
Although perhaps best known as causing food poisoning these toxins may act as specific allergens and induce IgE antibodies that may exacerbate the skin inflammation in AD (1-4). SEA and SEB are also implicated in infections, and may act as so-called superantigens, modulating and/or amplifying allergic inflammation (1, 5, 6).
S.a is harbored on the surface of the skin, and the secreted toxins are believed to penetrate the skin through the cutaneous lesions of AD (7). There is a 100 to 1000 times higher density of S.a colonies in the skin lesions compared with normal skin areas of patients with AD. In addition, a significantly higher frequency of colonies is found in apparently normal skin of patients with AD compared with skin of healthy subjects (1). The prevalence of S.a colonization in AD children has been reported to 93%, which is comparable to that in adults (8).
Circulating IgE antibodies to SEA and SEB are present in 50 to 85 % of patients with chronic AD (1, 6, 10). Titers of specific IgE to SEA and/or SEB has been correlated to severity of disease and density of S.a colonies in the skin (2, 9, 10). The sensitized patients had more severe AD; this correlation being more recognized in the age-group <7 years. Furthermore the patients who had both exotoxin producing S.a on their skin and IgE antibodies to the same toxin had significantly more severe AD. It is suggested that exotoxin specific IgE antibodies and exotoxin producing S.a should be measured at the same time to evaluate the effect of exotoxin on AD severity (9).
