Mechanisms underlying pyogenic bacterial infections of the skin

Pyogenic skin infections are commonly caused by Staphylococcus aureus (SA), Streptococcus pyogenes (GAS), and Pseudomonas aeruginosa (PA). Although these pathogens differ markedly in phylogeny, cell structure, and ecological adaptation, they converge on a coordinated pathogenic cascade encompassing adhesion, invasion, immune evasion, remodeling of the suppurative microenvironment, and nutrient acquisition. This review systematically compares the common pathological mechanisms underlying SA, GAS, and PA, while also delineating pathogen-specific virulence strategies of SA, GAS, and PA across key stages of infection, with representative molecular determinants including surface adhesins and coagulase in SA, M protein and streptokinase in GAS, and type IV pili and the Psl exopolysaccharide in PA. Particular focus is placed on how these bacteria evade complement- and phagocyte-mediated clearance, disrupt neutrophil function, remodel neutrophil extracellular traps (NETs) dynamics, alter coagulation-fibrinolysis balance, adapt to hypoxic lesions, and compete for restricted host nutrients. Although the three pathogens converge on pyogenic lesion formation as a shared pathological endpoint, they elicit distinct histopathological and clinical lesion phenotypes, including localized abscesses, rapidly progressive necrotizing soft-tissue infections, and chronic non-healing exudative wounds. These similarities and differences indicate that suppuration is not merely the endpoint of inflammation, but a dynamic pathogenic microenvironment jointly shaped by bacterial virulence and host responses. A clearer understanding of these common pathological axes and pathogen-specific differences provides a theoretical basis and new perspectives for the development of antibacterial and host-directed therapeutic strategies in pyogenic skin infections.