Staphylococcus aureus: salt stress, cell wall deficiency, and Biofílm formation

Abstract

Staphylococcus aureus (S. aureus) is a major cause of chronic infection and is of particular concern in the infection of implanted prostheses. Biofilm formation offers bacteria innate protection from antimicrobial agents and prevents the eradication of prosthetic infection in vivo. Current work shows a positive correlation between salt (NaCI) stress and cell wall deficiency in S. aureus. Cell wall deficient cells, produced in response to salt stress, demonstrate an increase in penicillin G resistance which increases with further salt stress, but returns to baseline levels after removal of the salt stress, indicating a phenotypic change in response to salt stress. Lysostaphin susceptibility decreases after salt stress, indicating changes to the structure of the cell wall in response to salt stress. Biofilm assays also show a positive correlation between biofilm formation and increased NaCI concentration. Further investigation using other Group I metals showed a positive correlation between increasing levels of KCl concentration and biofilm formation. This appears to be an ion specific effect related to potassium and sodium, as other Group I metals (Lithium, Rubidium and Caesium) did not have a similar effect. RT-PCR showed that both KCl and NaCI stress lead to a decrease in transcription of several genes, including some involved in cell wall synthesis, global gene regulation and polysaccharide intercellular adhesin production, over the baseline level. However, RT-PCR shows no significant difference between cells stressed with either KCl or NaCI. The work in this thesis shows a positive link between cell wall deficiency, antibiotic resistance and biofilm formation in S. aureus cells stressed with NaCI or KCl.