Staphylococcus Aureus Colonization In Atopic Dermatitis Patients

Background:Atopic dermatitis (AD) is a common chronic inflammatory skin disorder that induces several symptoms including pruritus and dryness, and is often associated with secondary cutaneous infections. AD is considered to be one of the most prevalent and studied skin diseases yet poorly understood, and its pathophysiology remains obscure. Even though other skin diseases (such as psoriasis) share the same pathologic factor -skin barrier defect - with atopic dermatitis, patients diagnosed with those diseases don't suffer infectious exacerbations like atopic patients do. Aim: Although many international researches have already discussed the relationship between staphylococcus aureus and AD, no studies about this subject in the Arabic region was documented. The aim of our study is to compare staphylococcus aureus colonization rates and densities between atopic dermatitis patients and non-atopic subjects, and to relate the colonization to the severity and duration of the disease. Materials and methods: This observational analytic study included 200 participants (99 diagnosed with atopic dermatitis and 101 control subjects without atopic dermatitis); nasal and skin swabs (lesional and non-lesional) were collected from patients, while nasal and only normal skin swabs were collected from controls. Positive swabs were assessed to determine the density of colonization. Results: 57.6% of patients had nasal colonization, 56.6% had lesional colonization and 30.3% had normal skin colonization. Nasal colonization rates and densities were higher in the patients group. We detected a correlation between colonization and severity of eczema, but no correlation between colonization and duration of the disease was detected. Conclusion: The high rates and densities of staphylococcus aureus colonization in lesional skin of atopic dermatitis patients point out the role of these organisms in the pathophysiology of the disease, put antibiotics on the treatment list of atopic dermatitis and explain infectious features in AD exacerbations.