As a member of the normal human skin microflora Staphylococcus epidermidis is considered to be non-pathogenic. However in recent years this species has often been associated with biomedical implant-related infections. Introduced via surgical sites from the skin of patients or hospital personnel, the bacteria are able to form so-called biofilms in vivo, multiple layers of cells that adhere to the surface of a solid substrate such as artificial heart valves, hip joints or interperitoneal catheters. The cell layers are surrounded by an extracellular 'slime' matrix that protects the cells from host immune responses and antibiotic agents, rendering the infections very difficult to treat once they are established. This can lead to systemic sepsis, particularly in immunocompromised patients. We therefore study the process of biofilm formation in vitro, in the hope that a better understanding of how biofilms form leads to theraputic means of preventing the formation of biofilms in vivo. Our molecular analysis of biofilm formation in S. epidermidis has lead to the identification of two gene operons that when mutated lead to a loss of biofilm formation in vitro. The intercellular adhesion ( ica ) operon mediates the production of sugar polymers that are responsible for cell-cell adhesion. This operon is likely to serve the same function in biofilm formation in other Staphylococcal species as well. The autolysin ( atl ) locus, shown in Staphylococcus aureus to be involved in cell separation. This operon seems to be involved in the adhesion of bacterial cells to solid substrates during biofilm formation in S. epidermidis and may bind to other biological molecules as well in vivo.
The accessory gene regulator ( agr ) operon in S. aureus has been shown to control a number of pathogenicity factors, including the internally encoded delta toxin. This operon is also present in S. epidermidis and it's role in regulating pathogenicity factors in this related species is under study.