Enviromental signals affecting ica-expression in Staphylococcus epidermidis

Abstract Staphylococcus epidermidis is a nosocomial pathogen, associated with infections of indwelling medical devices. The ability to adhere and form biofilms on biomaterial surfaces contributes to its virulence. Biofilm formation of S. epidermidis is influenced by the presence of polysaccharide intercellular adhesin, synthesized by proteins encoded in the icaADBC operon. The main aim of this thesis was to investigate the regulation of icaADBC gene expression during biofilm formation of clinical S. epidermidis isolates on different biomaterials and how environmental signals affect this regulation. Expression of ica is subject to phenotypic variation, which can result in heterogeneity in surface characteristics. Loss of ica was irreversible and independent of the mobile element IS256, indicating a new, unknown mechanism of phenotypic variation in clinical S. epidermidis isolates. In high frequency S. epidermidis switching strains, spontaneous mutations in lexA were found which resulted in deregulation of recA expression, as shown by real time PCR. Cinnamon oil is an effective antimicrobial agent to combat S. epidermidis biofilms, however its sub-MICs could induce biofilm formation in S. epidermidis. It is shown that ica-operon influence cell surface hydrophobicity, thermodynamics of adhesion, and biofilm formation in S. epidermidis strains, which is the interaction of ica-positive strains with the TC-PS surface was energetically favourable. It is concluded that the level of biomaterial-induced ica-expression does not correlate with the amount of biofilm formed, but initially aids bacteria in surviving antibiotic attacks. Once antibiotic treatment has started, the antibiotic itself induces slime production and if its concentration is high enough, killing results.