Abstract

Staphylococcus epidermidis is a major pathogen in nosocomial infections especially in immunocompromised patients1 . The majority of S. epidermidis infections are associated with the use of indwelling medical devices and it is suggested that the ability of S. epidermidis to generate biofilms on smooth surfaces contributes significantly to the pathogenesis of polymer associated infections. Recently, essential mechanisms of biofilm formation in S. epidermidis and S. aureus have been elucidated on the genetic and biochemical level. Thus, biofilm formation was found to depend on the presence and the expression of the icaADBC gene cluster which is involved in the production of an extracellular polysaccharide adhesin (PIA)2,3,4 . The PIA mediates the contact of the bacterial cells to each other and bacteria become embedded in this slimy matrix during the accumulative phase of biofilm formation4. The ica operon was found to be widespread in S. epidermidis multiresistant isolates causing polymer-associated infections and its expression was shown to undergo strong phenotypic variation5. This work summarizes genetic mechanisms which contribute to an altered ica

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