Bacterial conjunctivitis occupies a significant place among infectious diseases of the anterior segment of the eye, and within its etiological spectrum, Staphylococcus aureus is recognized as a particularly relevant pathogen, especially in adults, elderly individuals, and patients with compromised ocular surface defense mechanisms. Contemporary literature indicates that the pathogenicity of this microorganism is not limited to superficial colonization but is mediated through a complex, multi-component virulence system. The adhesion of S. aureus to the conjunctival surface is facilitated by fibronectin-binding proteins, extracellular adherence protein, and clumping factors; subsequently, biofilm formation, tissue invasion, toxin secretion, and immune evasion mechanisms contribute to the persistence and recurrence of the disease. In particular, alpha-toxin, gamma-toxin, Panton–Valentine leukocidin, and enterotoxins enhance epithelial cell damage, promote the release of inflammatory mediators, and intensify local tissue destruction. Molecular studies have demonstrated a high prevalence of genes associated with adhesion, invasion, and immune evasion in ocular S. aureus strains; in certain clinical series, the hld and hlg genes were detected significantly more frequently in infectious strains compared to non-infectious isolates. Recent observations indicate that the proportion of staphylococci in bacterial conjunctivitis and the issue of methicillin-resistant strains remain persistent, thereby limiting the effectiveness of empirical therapy. Thus, the pathogenesis of S. aureus-associated bacterial conjunctivitis should be considered as an integrated system involving adhesion, biofilm formation, toxic injury, induction of inflammation, and antibiotic resistance.

Bacterial conjunctivitis, Staphylococcus aureus, pathogenesis, virulence factors, adhesion, biofilm, alpha-toxin, gamma-toxin, Panton–Valentine leukocidin, enterotoxin B, antibiotic resistance, MRSA, conjunctival inflammation.

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