In the era of invasive medicine health-care associated infections with Staphylococcus aureus belong to the most prevalent and deleterious side effects of surgery which lead to significant morbidity and illness after admittance to a hospital (hospital infections = “nosocomial infections”).
Today S. aureus is no longer regarded exclusively as an extracellular pathogen: it has been shown that S. aureus is endocytosed by a number of non-professional phagocytes (e.g. endothelial cells, epithelial cells, osteoblasts, and fibroblasts). This “invasion” of body cells may represent a strategy for the bacteria to escape the immune system.
Bacteria-containing phagosomes often fuse with lysosomes. Within these resulting phagolysosomes bacteria are efficiently digested. However, staphylococci can either i) persist in the infected cells for extended periods (several days / months) as so-called small-colony variants or ii) break out of the phagolysosome. The latter, also termed "phagosomal ecape", leads to a translocation of S. aureus into the host cell cytoplasm, where it replicates and readily kills host cells. In the Staphylococcus-centric projects investigated at the Chair of Microbiology we want to understand this alternative intracellular virulence of S. aureus.