Clinicians have long since been aware that bacteria and other microorganisms play a role in the etiology of atopic dermatitis. Indeed, the immunological profile of atopy favors colonization by Staphylococcus aureus, and the bacteria are present in most patients with atopic dermatitis, even in the absence of skin lesions. Clinical signs of impetiginization, such as weeping and crusting, periauricular fissuration, or small superficial pustules are a sensitive indicator that the numbers of S. aureus may have increased and a clinical indication of secondary infected dermatitis. However, recent research that has focussed on the role of S. aureus in atopic dermatitis, offers a reversed perspective, by presenting evidence that the underlying pathology of atopic dermatitis, i.e. an alteration of the skin barrier and inflammation of the upper dermis, depends itself on the presence of an infectious process. In other words, secondary infection with S. aureus emerges as a cause of atopic dermatitis. Secondary infections due to fungi have, comparatively, received less attention, but there is evidence for a role for Malassezia spp. as a factor in dermatitis with a head and neck distribution pattern. Viral infections, such as herpes simplex virus, and mixed infections of intertriginous spaces, may complicate an underlying atopic dermatitis, but are not perceived as etiologic factors. Recent research has greatly contributed to our understanding of the pathophysiological potential of S.aureus superantigens in atopic dermatitis, suggesting that antibiotic therapy might be an important element in the therapeutic management of atopic dermatitis. At present, however, the clinical evidence is scarce with regards to demonstrating a clear advantage of combined anti-inflammatory and antibiotic treatment, compared with anti-inflammatory treatment alone. If there is a consensus that the presence of clinically infected lesions in atopic dermatitis warrants a course of specific antibiotic topical therapy, the clinical benefit of antibiotic agents in apparently uninfected atopic dermatitis, as present in the majority of patients, remains an open question.Moreover, the impact of adjuvant skin care on the cutaneous microflora needs to be quantified in order to properly assess the role of specific antibiotic therapy in clinically uninfected atopic dermatitis. In the meantime, secondary infections in atopic dermatitis remain a secondary problem in clinical atopic dermatitis management, and specific anti-infective therapy remains a method of fine-tuning for optimizing individual atopic dermatitis treatment.