Aetiology

Cellulitis develops when micro-organisms gain entry to the dermal and subcutaneous tissues via disruptions in the cutaneous barrier. Beta-haemolytic streptococci and Staphylococcus aureus are most commonly implicated as the causative agents of cellulitis.[6][7][8][9][10][11]​​​​​ However, other micro-organisms can uncommonly result in cellulitis. Usually this occurs in a host with altered immunity or as the result of a specific exposure (e.g., aquatic environment, or animal or human bite).[12]​ Such organisms include Pseudomonas aeruginosa, Pasteurella multocida, Capnocytophaga canimorsus, Vibrio vulnificus, and Cryptococcus neoformans.[12]​[13]​​[14]​ Non-purulent cellulitis is most commonly due to beta-haemolytic streptococci.[15]

Pathophysiology

The pathophysiology of cellulitis has not been well studied. The burden of organisms in cellulitis appears to be low.[12]​ Some have speculated that the pyrogenic exotoxins produced by beta-haemolytic streptococci may contribute to the clinical findings in cellulitis.[16]​ There is evidence of local production of inflammatory cytokines by keratinocytes.[17] Interaction between surface proteins of Streptococcus pyogenes and adhesions on the surface of keratinocytes and Langerhans cells may be a requirement for infection to develop.[18] Common mechanisms of a break in skin barrier include lacerations, bite wounds, instrumentation (e.g., needles), pre-existing skin conditions, and surgery.[16] In many instances, tinea pedis may cause a disruption in the cutaneous barrier and allow entry to offending bacterial organisms.[19]

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