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Background  In recent years,  Staphylococcus epidermidis  (  Se ) has become a major nosocomial pathogen and the most common cause of infections of implanted prostheses and other indwelling devices. This is due in part to avid biofilm formation by  Se  on device surfaces. However, it still remains unknown that how the process of  Se  biofilm development is associated with relapsed infection in such patients.    Results  We have identified clinical  Se  isolates displaying enhanced biofilm dispersal and self-renewal relative to reference strain. These isolates also exhibit enhanced initial cell attachment, extracellular DNA release, cell autolysis and thicker microcolonies during biofilm development relative to reference strain. Our genetic analyses suggest that these clinical isolates exhibit significant downregulation of  RNAIII , the effector molecule of the  agr  quorum sensing system, and upregulation of the autolysin gene  atlE . Isogenic deletion of the  agr  system in  Se  1457 confirmed that  agr  negatively regulating  atlE  resulted in enhanced initial cell attachment, extracellular DNA release, cell autolysis and biofilm formation abilities. In contrast, double deletion of  agr  and  atlE  significantly abolished these features.    Conclusions  Collectively, these data reveal the role of  agr  system in long-term biofilm development and pathogenesis during  Se  caused indwelling devices-related relapsed infection.

Staphylococcus epidermidis recovered from indwelling catheters exhibit enhanced biofilm dispersal and “self-renewal” through downregulation of agr