Additional study findings indicated that patients with AD had a significantly higher risk for S. aureus colonization of lesional skin as compared with those without AD.
Although patients with atopic dermatitis (AD) have long been known to experience Staphylococcus aureus (S. aureus) colonization in their skin, new data suggest that these patients show an increased risk of colonization compared with those without AD, and that the prevalence of colonization increases as the severity of AD increases, according to the results of a study recently published in the British Journal of Dermatology.1
First author, Joan E. E. Totté, MD, from the Department of Dermatology at the Erasmus MC University Medical Centre in Rotterdam, and her colleagues conducted a systematic literature search and subsequent meta-analysis of the collected data using a random-effects model to determine pooled estimates of the prevalence of S. aureus colonization in patients with AD, as well as the risk of colonization in comparison to those without AD. The literature search included experimental and observational original studies involving patients of all ages with a diagnosis of AD confirmed by a physician, written in any language, and published at any time.
When asked about the study rationale, Dr. Totté told Contagion, "In the available literature, the reported prevalences of colonization of the skin and nose with S. aureus vary widely in patients with atopic dermatitis. By performing this study, we tried to define the prevalence of S. aureus skin and mucosal colonization in patients with AD, to get more insight in the importance of the bacterium in the disease."
The results of the systematic literature search yielded 95 observational studies, 30 of which had control groups. Most of the included studies were determined to be of fair to poor quality, and heterogeneity was high (>85%) regarding the pooled prevalence of nasal and skin colonization. According to the results of the random-effects model employed, the pooled prevalence of S. aureus colonization among patients was 70% (95% CI 66—74) for lesional skin, 39% (95% CI 31–47) for nonlesional skin and 62% (95% CI 57–68) for the nose. In lesional skin, the prevalence of colonization was shown to increase with increasing disease severity (1.02, 95% CI 0.21–1.82). Furthermore, an analysis of the subgroup of studies that examined patients with mild AD showed roughly half of the pooled prevalence of skin colonization (43%, 95% CI 31–57) as compared to that derived from studies of patients with severe AD (83%, 95% CI 74–89).
Additional study findings indicated that patients with AD had a significantly higher risk for S. aureus colonization of lesional skin as compared with those without AD (odds ratio [OR] 19.74, 95% confidence interval [CI] 10.88—35.81, P <0.001). Although smaller, the risks of colonization in nonlesional skin (OR 7 77, 95% CI 3 82—15 82, P <0.001) and in the nose (OR 4.50, 95% CI 3.00—6.75, P <0.001) were also significantly greater than risks assessed for those without AD.
In describing her interpretation of the study data, Dr. Totté told Contagion, "This systematic review confirms a high abundance of S. aureus on the skin and in the nose in patients with AD compared to healthy people. Thereby it shows that colonization increases in cases of more severe AD. Some studies describe a causal role of S. aureus in AD. However, there is no clear evidence yet for the added value of anti- S. aureus therapy in AD." According to the authors, "These results provide an indication of the importance of colonization as a factor in the pathogenesis of AD and encourage evaluation of targeted antistaphylococcal therapy for the skin (and nose), for example based on the use of anti-S. aureus lysins."
Regarding the broader implications of the study results, Dr. Totté and colleagues said that, "Additional examination of colonization in patients with different phenotypes (sensitized and nonsensitized, early onset vs. late onset) might provide insight into the type of patients who are likely to benefit most from targeted therapy against S. aureus." Dr. Totté told Contagion, "In my opinion, the results of this systematic review encourage reevaluation of the added value of anti-S. aureus therapy in patients with more severe AD in well set up randomized clinical studies."
William Perlman, PhD, CMPP is a former research scientist currently working as a medical/scientific content development specialist. He earned his BA in Psychology from Johns Hopkins University, his PhD in Neuroscience at UCLA, and completed three years of postdoctoral fellowship in the Neuropathology Section of the Clinical Brain Disorders Branch of the National Institute of Mental Health.