Erysipelas pathophysiology

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Luke Rusowicz-Orazem, B.S.


Erysipelas develops from epidermal penetration of streptococcal bacteria, usually the group A streptococcus Streptococcus pyogenes.The infection occurs upon the binding of superficial ligands to the epidermal receptor cells. Dermal damages, including abrasions or lesions, allow the pathogen to adhere without being removed by natural exfoliation. A myriad of virulence factors causes bacteria to adhere to the dermis. Upon adhesion, Streptococcus pyogenes begin to invade through expression of M protein or fibronectin-binding protein. Phagocytosis is inhibited by the bacteria due to the binding of factor H and the binding of fibrinogen on the surface of the M protein. Colonization of the bacteria begins; erysipelas develops from the inflammatory response of the increased volume of leukocytes at the point of infection. The streptococcal pyrogenic exotoxins release large amounts of cytokines that result in tissue damage characteristic of erysipelas. There is evidence of genetic predisposition and susceptibility to erysipelas in individuals with streptococcal infection. Erysipelas is associated with the following conditions associated with group A streptococcal infection, including cellulitis, necrotizing fasciitis, and toxic shock syndrome.


Erysipelas develops from exotoxins released due to epidermal penetration of the pathogenic bacteria.


There is evidence of increased susceptibility to erysipelas in individuals with streptococcal infection, due to the following genetic factors:[14]

Associated Conditions

Erysipelas is associated with the following streptococcal conditions:[15]


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