Background/Objectives: Children with atopic dermatitis often have infective exacerbations which are treated with antibiotics and/or antiseptics. The most common infective cause is Staphylococcus aureus with a worldwide trend towards antibiotic resistance. This prospective observational audit aimed primarily to establish the prevalence of S. aureus colonisation in New Zealand children with atopic dermatitis attending a specialised paediatric dermatology clinic. Secondary aims were to assess whether S. aureus colonisation correlated to clinical severity, the sensitivity patterns to antibiotics (in particular methicillin-resistant S. aureus, and to identify any demographic or management risk factors.
Methods: Subjects were children aged 18 years or younger attending a tertiary public hospital dermatology clinic with a diagnosis of atopic dermatitis. Demographic and social data, as well as current and previous systemic and topical treatments, were recorded. Patients were examined and the extent of atopic dermatitis determined using a standardised scale (Scoring Atopic Dermatitis (SCORAD)). Two skin swabs were taken for culture and standard sensitivities; one from the left antecubital fossa and one from the worst area of atopic dermatitis. Microbiological cultures and density of S. aureus colonisation were recorded. SCORAD and density of S. aureus culture were correlated. Demographic and clinical data from children with S. aureus was analysed.
Results: One hundred children were recruited from March 2007 to May 2008. S. aureus was isolated from68 patients. There was a positive correlation between the density of S. aureus culture and severity of SCORAD (Spearman r = 0.55, P < 0.0001). There was also a positive, though weaker, correlation between SCORAD and ethnicity with Māori /Polynesian children generally having more severe atopic dermatitis (r = 0.22, P = 0.028). Although a greater proportion of Māori or Pacific Island children were colonised by S. aureus than other ethnic groups this did not reach statistical significance (78% and 60%, respectively, P = 0.0842). There was no significant correlation between either S. aureus prevalence or its density and age (r = 0.09, P = 0.39 and r = 0.12, P = 0.23, respectively). There were no significant differences in sex or treatments (use of antibiotics, antiseptics, calcineurin inhibitors, emollients or corticosteroids) between S. aureus-positive and S. aureus-negative children. Only 12 S. aureus-positive children demonstrated antibiotic resistance, 10 to erythromycin and only two to flucloxacillin.
Conclusions: Three quarters of children with atopic dermatitis have at least one positive culture, of which the vast majority is S. aureus. The density of S. aureus colonisation correlates to severity of atopic dermatitis. Children who are S. aureus culture-positive had no significant demographic or clinical features different to children who were culture-negative. Only two children grew S. aureus resistant to flucloxacillin (2% resistance rate), which remains the ideal first line of treatment in our local population.