Summary
It has become clear that Staphylococcus aureus is a facultative intracellular microorganism. Adherence and invasion are a prerequisite
for endovascular infections caused by S. aureus, such as infective endocarditis. These
phenomena may also be involved in the pathogenesis of invasive and metastatic infection
upon hematogenous dissemination, such as osteomyelitis and abscess formation. The
underlying molecular mechanism has been elucidated in detail, including its likely
relevance in vivo. However, the mode of action of recently identified modulators of
invasion, such as pls/Pls have not yet been clarified. The potential outcome for host
cells and S. aureus following invasion are diverse. Surprisingly, induction of apoptosis
in human endothelial cells is more complex than previously thought, since it appears
to involve multiple virulence factors. In the light of increasing resistance to antimicrobial
therapy, understanding the multifacetted pathogenesis of S. aureus infection in detail
is needed for a better prevention and therapy.
Keywords
Bacterial invasion - host cells -
Staphylococcus aureus
- infective endocarditis - pathogenesis