ISSN: 2155-9554
Gomes PLR, Gathsaurie Neelika Malavige, Fernando N, Mahendra MHR, Seneviratne JKK and Graham S Ogg
Background:Staphylococcus aureus colonizes most patients with atopic dermatitis. Staphylococcus aureus is able to produce staphylococcal enterotoxins, staphylococcal enterotoxin-like toxins and Toxic shock syndrome toxin – 1.The presence of superantigen encoding genes has been associated with atopic dermatitis in other cohorts.
Aim: To determine the association of different Staphylococcal superantigens with clinical disease severity in a tropical disease setting in patients with atopic dermatitis.
Methodology: Skin swabs collected from 100 patients with atopic dermatitis and 120 controls were cultured. Severity of atopic dermatitis was graded using the Nottingham Eczema Severity Score. Bacterial DNA was extracted and superantigen genes were detected by separate PCRs.
Results:52/59 (88%) of Staphylococcus aureus isolates from patients and 5/16 (31%) from healthy individuals had genes encoding at least one type of superantigen. Each superantigen type was expressed significantly higher (P<0.05) in patients than in healthy individuals. Possession of genes for staphylococcal enterotoxin-like toxin type M (P=0.038) and staphylococcal enterotoxin-like toxin type O (P=0.016) were associated with milder disease. Possession of staphylococcal enterotoxin type B gene was significantly higher (p=0.0186) in Staphylococcus aureus isolated from patients who were aged 5 years or older compared to Staphylococcus aureus isolated from younger patients. Strains possessing genes that encode the classical superantigens such as staphylococcal enterotoxin type A, B, C, E and Toxic shock syndrome toxin – 1 were significantly associated with patients with moderate to severe disease when they possessed not more than two superantigen genes in total.
Conclusions: Superantigens associate with atopic dermatitis in a cohort of patients from Sri Lanka consistent with a role in disease pathogenesis. Differences in superantigen gene possession are unlikely to explain differences in disease prevalence between populations from tropical and temperate climates.