The Pathogenicity Mechanisms of Staphylococcus aureus

Staphylococcus aureus is one of the most important bacterial pathogens affecting both humans and animals. This review discusses the most significant factors that contribute to the pathogenicity of these bacteria and the mechanisms that regulate their expression. We also focus on the factors that play a role in the pathogenesis of skin diseases. S. aureus possesses a wide array of virulence factors that allow it to bypass passive and active mechanisms of the host's immune system and effectively infect and spread within the infected organism. These include factors that facilitate colonization of the skin (i.e., arginine catabolic mobile element-ACME), mucous membranes and other surfaces, proteins protecting the bacteria from the host's immune system, superantigens and superantigen-like proteins, surface proteins that promote adhesion and biofilm formation, toxins, enzymes, and iron uptake systems. Additionally, a complex network of regulatory systems (accessory gene regulator -Agr, (staphylococcal accessory regulator -Sar, S. aureus exoprotein expression -Sae, and others) controls the expression of virulence genes at the transcriptional and translational levels. The activity of these regulatory systems is pivotal in determining whether S. aureus initiates an invasive infection, characterized by toxin and enzyme production (e.g., hemolysin alpha -Hla, phenol soluble modulins -PSM, toxic shock syndrome -TSST-1, enterotoxins, Panton-Valentine leukotoxin- PVL). This is indicative of community-acquired S. aureus (CA-Sa, CA-MRSA, CA-MSSA), or a chronic infection, characterized by surface protein expression and biofilm formation, which is indicative of hospital-acquired or healthcare-acquired S. aureus (HA-Sa, HA-MRSA, HA-MSSA).