Erysipelas pathophysiology On the Web
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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.
- Group A streptococcal infection causes erysipelas upon infiltration of the epidermis through a skin abrasion or lesion.
- The streptococcal infection occurs upon the binding of superficial ligands to the epidermal receptor cells.
- Epidermal damages, including abrasions or lesions, allow the pathogen to adhere without being removed by natural exfoliation.
- Streptococcus pyogenes adheres to the dermis due to the following virulence factors:
- Containing M protein, allowing colonization
- Lipotechoic acid (LTA): binds with fibronectin or fibrinogen, causing adhesion of the bacteria to the dermis
- Protein F: binds with fibronectin to mediate adhesion
- 29-kDa fibronectin-binding protein
- Glyceraldehyde 3-phosphate dehydrogenase
- 70-kDa galactose-binding protein
- Vitronectin-binding S protein
- Collagen-binding protein
- Serum opacity factor
- Hyaluronate capsule
- 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.
- Human leukocyte antigen (HLA) Class II and T-cell receptor Vβ variation can cause differing susceptibility due to their influence on Super antigen production, contributing the to severity of cytokine release from inflammation.
- The region Angiotensin II receptory type 1 (AGRT1) on the chromosome 3q22 has been shown to reveal susceptibility to developing erysipelas by determining an individual's cytokine response to Streptococcus pyogenes infection.
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