The altered skin structure of people with atopic predisposition allows increased penetration of allergens and irritative substances (Roll et al., 2004; Hudson 2006). Many studies have shown that the extent of S. aureus colonization correlates with AD disease activity (Cho et al., 2001; Biedermann 2006). In more than 90% of AD patients, a massive skin colonization with S. aureus (up to 107cfu/cm2 of lesional skin) can be found (Matsui et al., 2000). A prerequisite for bacterial colonisation are the genuine barrier dysfunction, mechanical disruption of the barrier and trigger of inflammation (scratching), alkaline pH, decreased IgA secretion through sweat production, predominant Th2 cells inhibiting anti-infectious immune responses, and reduced antimicrobial peptides, all representing important pathophysiological features leading to the disruption of the primary skin defense system (Biedermann et al. 2001; Biedermann&Röcken 2001,; Biedermann et al. 2002; Biedermann 2006; Howell, 2005; Rieg 2005).