Staphylococcus aureus

Staphylococcus aureus represents one of humanity's most persistent bacterial adversaries, combining biofilm expertise with remarkable genetic adaptability. In chronic wounds, S. aureus frequently coexists with Pseudomonas aeruginosa in polymicrobial biofilms—complex communities where the two species engage in chemical warfare while simultaneously benefiting from each other's presence. Pseudomonas produces compounds that kill planktonic S. aureus, yet S. aureus persists in biofilms by entering small colony variant states that resist these attacks.

This coexistence creates treatment challenges far exceeding either species alone. S. aureus biofilms shelter within extracellular matrices that block antibiotics and immune cells. The bacteria communicate through the accessory gene regulator (agr) quorum sensing system, coordinating virulence factor production based on population density. At low densities, cells adhere and colonize; at high densities, they produce toxins and disperse. This density-dependent behavioral switch optimizes strategy for each growth phase.

MRSA—methicillin-resistant S. aureus—demonstrates how horizontal gene transfer reshapes competitive landscapes. The mecA gene encoding methicillin resistance was acquired from coagulase-negative staphylococci, likely in a healthcare setting where antibiotic pressure was intense. This single acquisition transformed S. aureus from manageable pathogen to existential threat. The bacterium's ability to form biofilms on medical devices, combined with antibiotic resistance and immune evasion capabilities, makes it the paradigmatic hospital-adapted pathogen. Understanding S. aureus requires understanding how organisms build defensive infrastructure while maintaining offensive capabilities.