Staphylococcal enterotoxin B

 
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Code: m81
Latin name: Staphylococcus aureus
It is a major clinical problem to identify the extent to which a mold-sensitive patient's symptoms can be attributed to IgE-mediated allergy.

Allergen Exposure

Patients with atopic dermatitis (AD) are frequently colonized with Staphylococcus aureus (S.a) strains that secret exotoxins such as Staphylococcus 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.

Potential Cross-Reactivity

No information available.

Clinical Experience

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). 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).
 
Review
Patients with atopic dermatitis (AD) are frequently colonized with Staphylococcus aureus (S.a) strains that secret exotoxins such as Staphylococcus 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). 

References

  1. Nissen D, Pedersen LJ, Skov PS, Vejlsgaard GL, Poulsen LK, Jarlov JO, et al. IgE-binding components of staphylococcal enterotoxins in patients with atopic dermatitis. Ann Allergy Asthma Immunol 1997;79(5):403-8.
  2. Bunikowski R, Mielke M, Skarabis H, Herz U, Bergmann RL, Wahn U, et al. Prevalence and role of serum IgE antibodies to the Staphylococcus aureus-derived superantigens SEA and SEB in children with atopic dermatitis. J Allergy Clin Immunol 1999;103(1 Pt 1):119-24.
  3. Leung DY, Harbeck R, Bina P, Reiser RF, Yang E, Norris DA, et al. Presence of IgE antibodies to staphylococcal exotoxins on the skin of patients with atopic dermatitis. Evidence for a new group of allergens. J Clin Invest 1993;92(3):1374-80.
  4. Neuber K, Steinrucke K, Ring J. Staphylococcal enterotoxin B affects in vitro IgE synthesis, interferon- gamma, interleukin-4 and interleukin-5 production in atopic eczema. Int Arch Allergy Immunol 1995;107(1-3):179-82.
  5. Neuber K, Konig W. Effects of Staphylococcus aureus cell wall products (teichoic acid, peptidoglycan) and enterotoxin B on immunoglobulin (IgE, IgA, IgG) synthesis and CD23 expression in patients with atopic dermatitis. Immunology 1992;75(1):23-8.
  6. Konig B, Neuber K, Konig W. Responsiveness of peripheral blood mononuclear cells from normal and atopic donors to microbial superantigens. Int Arch Allergy Immunol 1995;106(2):124-33.
  7. Yudate T, Yamada H, Tezuka T. Role of staphylococcal enterotoxins in pathogenesis of atopic dermatitis: growth and expression of T cell receptor V beta of peripheral blood mononuclear cells stimulated by enterotoxins A and B. J Dermatol Sci 1996;13(1):63-70.
  8. Hoeger PH, Lenz W, Boutonnier A, Fournier JM. Staphylococcal skin colonization in children with atopic dermatitis: prevalence, persistence, and transmission of toxigenic and nontoxigenic strains. J Infect Dis 1992;165(6):1064-8.
  9. Nomura I, Tanaka K, Tomita H, Katsunuma T, Ohya Y, Ikeda N, et al. Evaluation of the staphylococcal exotoxins and their specific IgE in childhood atopic dermatitis. J Allergy Clin Immunol 1999;104(2 Pt 1):441-6.
  10. Tada J, Toi Y, Akiyama H, Arata J, Kato H. Presence of specific IgE antibodies to staphylococcal enterotoxins in patients with atopic dermatitis. Eur J Dermatol 1996;6(8):552-4.

As in all diagnostic testing, the diagnosis is made by the physican based on both test results and the patient history.