Staphylococcus aureus causes a wide spectrum of infections in humans. Virulence in S. aureus is mediated by cell wall-associated and secreted proteins. Cell wall-associated proteins enable the bacteria to adhere to tissue components. Our studies have focused on the contribution to virulence of bacterial surface adhesins, such as the fibrinogen-binding protein, or clumping factor A (ClfA), and the fibronectin-binding protein A (FnbA), using a gene transfer approach. Our current work addressed how these proteins interact in the initiation and further development of the infection process.
Cell wall biochemistry
The cell wall biochemistry group is interested in the structural-inflammatory relationship of Gram-positive bacterial cell walls. Purified cell walls are biochemically characterised by various methods (including high performance liquid chromatography and mass spectrometry) and their inflammatory activity determined in an ex vivo model.
In addition, in collaboration with the antimicrobial agents and pathogenesis groups, these analytical techniques are used to study the cell wall structure bacteria in exposed to antibiotics, and a FACS is used to determine protein-receptor interactions.
Ecology and evolution of staphylococci
We are studying transfer mechanisms and population biology of SCCmec element which confers high-level antibiotic resistance to S. aureus but is also commonly found in other less-pathogenic staphylococci, such as S. epidermidis.
Genomic microarrays and whole genome sequencing of S. aureus isolated from various hosts are currently used to assess genetic diversity and subsequently attempt to identify the genetic determinants necessary for colonization of humans.