10 Chapter 1 Introduction and outline of the thesis Staphylococcus aureus is a fascinating pathogen. The Gram-positive spherically shaped bacterium is generally considered as the most virulent member of the Staphylococcus genus [1]. It adopted its name in the 1880s from the combination of the Greek words staphyle (bunch of grapes), kokkos (berry), and the Latin word aureum (gold), representing the appearance of the colonies on blood agar plates [2, 3]. As a human commensal, it colonizes more than half of the population, either intermittently or persistently [4]. Colonized persons are often asymptomatic and can be colonized in the anterior nares, throat, groin, skin, intestine, and other body sites. In only a minority, S. aureus causes disease – often caused by the individual’s colonizing strain [5]. S. aureus is the causative agent of common and relatively benign infections such as folliculitis and impetigo. On the other end of the clinical spectrum, it is the causative agent of severe invasive infections such as endocarditis, spondylodiscitis, and bacteremia (Figure 1), and even the leading cause of mortality by bloodstream infections worldwide [6]. Figure 1. A glimpse of the spectrum of clinical manifestations of Staphylococcus aureus The variability in both colonization and invasive infection of S. aureus is the result of a complex interplay between host, pathogen, and environment. Many aspects of these interactions are largely unexplained. Susceptibility of the host is, among other factors, influenced by age, immune response and genetic make-up. Although predisposing factors in the host have been identified, it remains impossible to predict who will be colonized, who will develop disease and in whom this disease will be severe.
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