Patients with atopic dermatitis (AD) have an increased risk of bacterial skin infections, which cause significant morbidity and, if untreated, may become systemic. Staphylococcus aureus colonizes the skin of most patients with AD and is the most common organism to cause infections. Overt bacterial infection is easily recognized by the appearance of weeping lesions, honey-coloured crusts and pustules. However, the wide variability in clinical presentation of bacterial infection in AD and the inherent features of ADcutaneous erythema and warmth, oozing associated with oedema, and regional lymphadenopathyoverlap with those of infection, making clinical diagnosis challenging. Furthermore, some features may be masked because of anatomical site-and skin-type-specific features, and the high frequency of S. aureus colonization in AD makes positive skin swab culture of suspected infection unreliable as a diagnostic tool. The host mechanisms and microbial virulence factors that underlie S. aureus colonization and infection in AD are incompletely understood. The aim of this article is to present the latest evidence from animal and human studies, including recent microbiome research, to define the clinical features of bacterial infections in AD, and to summarize our current understanding of the host and bacterial factors that influence microbial colonization and virulence. The role of bacterial skin infections in atopic dermatitis, H. Alexander et al. 1335 Fig 6. Hypothetical damage-response framework for Staphylococcus aureus in atopic dermatitis (AD). 82 Different host-S. aureus interactions result in different damage-response relationships. Curves A and B represent the damage-response relationships of S. aureus with two different hosts or those of a single host with two different S. aureus strains. The outcome for the host depends on the strength of the host response to S. aureus or the virulence of S. aureus. During intermediate host responses neither interaction (A or B) causes clinical evidence of infection, as the amount of damage incurred by the host is insufficient (1). However, in the setting of weak or strong responses both interactions cause an AD flare (2) and interaction B causes overtly infected AD (3). The position of the curve is determined by multiple host and S. aureus factors.