| Popis: |
Publisher Summary This chapter discusses the methods to detect and analyze phenotypic variation in biofilm-forming staphylococci. Staphylococci are the most common cause of medical device-associated infections, especially in immunocompromised patients. The pathogenesis of these infections is favored by the ability of certain Staphylococcus epidermidis and Staphylococcus aureus strains to express a slimy matrix, in which the bacteria becomes embedded and forms thick, multilayered biofilms on smooth surfaces. Staphylococcus aureus and S. epidermidis clinical isolates are known to vary in a wide range of phenotypic properties. Thus, it has been shown that cells from a single parental clone can differ in terms of growth rate, exoprotein production, antibiotic susceptibility, and adhesion. It has been suggested that this phenotypic variation might contribute to the successful adaptation of the bacteria to environmental changes. With respect to S. epidermidis , it was shown that the majority of the clinical S. epidermidis isolates grow in multicellular clusters and that the removal of these biofilms (for example, by antibiotics) is difficult. Therefore, it is assumed that staphylococcal biofilm formation represents an advantage for the bacteria that contributes considerably to pathogenesis. However, numerous studies give evidence that S. epidermidis has a strong capacity to vary biofilm expression. Thus, it was observed that within a S. epidermidis biofilm population biofilm-negative variants are currently released. This chapter describes the detection and genetic analysis of these biofilm-negative variants. It shows the application of the 16S rRNA in situ hybridization technique for the detection of staphylococci grown in biofilms, and in infected tissues. |
