S. aureus is capable of causing both local and systemic diseases, with significant morbidity and mortality. Bloodstream bacteraemia caused by S. aureus is one of the most serious common infections worldwide. The fact that S. aureus is able to develop multidrug resistance and survive a course of antibiotics has renewed interest in elucidating host defence mechanisms. We work to enhance the understanding of the determinants of S. aureus infection. The zebrafish infection model has been established for the purpose of in vivo study (Prajsnar et al 2008). Embryos are transparent which facilitates imaging of interaction between pathogen and host innate immune system. We observe how infection progresses continuously within a living organism, and how different time points engage different features of pathogen strategy and host defence. Bacterial dynamics are stable in the first few hours of infection and as phagocytes reach capacity, bacteria remain inactive before dissemination occurs.
We have recently shown that phagocytes support the foundation of disseminated infection from a very small number of bactgeria (Prajsnar et al 2012). We now aim to explain what is causing this phenomenon and how can we apply this knowledge in order to develop new therapeutic or prophylactic approaches.