Staphylococcus aureus: A Review of the Pathogenesis and Virulence Mechanisms

Abstract

Staphylococcus aureus is a formidable human pathogen responsible for infections ranging from superficial skin lesions to life-threatening systemic diseases. This review synthesizes current knowledge on its pathogenesis, emphasizing colonization dynamics, virulence mechanisms, biofilm formation, and antibiotic resistance. By analyzing studies from PubMed, Scopus, and Web of Science, we highlight the pathogen's adaptability, driven by surface adhesins (e.g., ClfB, SasG), secreted toxins (e.g., PVL, TSST-1), and metabolic flexibility in iron acquisition and amino acid utilization. Nasal, skin, and oropharyngeal colonization are reservoirs for invasive infections, with biofilm persistence and horizontal gene transfer exacerbating antimicrobial resistance, particularly in methicillin-resistant S. aureus (MRSA). The review underscores the clinical challenges of multidrug-resistant strains, including vancomycin resistance and decolonization strategies' failure to target single anatomical sites. Key discussions address host-microbiome interactions, immune evasion tactics, and the limitations of current therapies. Future directions advocate for novel anti-virulence therapies, multi-epitope vaccines, and AI-driven diagnostics to combat evolving resistance. Strengthening global surveillance and interdisciplinary collaboration is critical to mitigating the public health burden of S. aureus.

Keywords: MRSA; Staphylococcus aureus; antibiotic resistance; biofilm formation; colonization dynamics; metabolic adaptation; virulence factors.

Figure 1

Host–Epithelium Interaction with S. aureus: mechanisms of colonization and barrier disruption. Legend: Throat and Oropharynx: S. aureus adheres to the ciliated epithelium, leading to barrier disruption and potential infection. Nasal Epithelium: S. aureus colonizes the nasal mucosa, aided by teichoic acid and microbial surface components recognizing adhesive matrix molecules (CHiB). Skin: The bacterium interacts with the epidermis, using adhesins like SasG and ClfB to bind to skin components and cause inflammation. Intestinal Epithelium: S. aureus adheres to the intestinal mucosa, producing toxins and mucus-associated proteins that facilitate colonization.

Figure 2

Regulation of virulence factors in S. aureus by agr QS.