Mechanisms for the increased Staphylococcus aureus colonization in atopic eczema are only partially known. From the aspect of the bacterium, the presence of various extracellular matrix components seems important. In the host epidermal lipid deficencies disturbing barrier dysfunction are important. Staphylococcus aureus' immunological and inflammatory effects include the release of superantigens, additional exotoxins and exoenzymes and perhaps bacterial DNA-triggered mechanisms. Therapeutic possibilities include the use of systemic antibiotics in cases of generalized superinfected atopic eczema, the use of corticosteroids and specific antibiotic-antiseptic combinations in cases of localised superinfected atopic eczema and the wide-spread use of topical antiseptics in cases of microbial-laden atopic eczema.