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.
Overview
Historically, the face was most affected; today the legs are affected most often. Erysipelas infections can enter the skin through minor trauma, eczema, surgical incisions and ulcers, and often originate from strep bacteria in the subject's own nasal passages.
Pathogenesis
Erysipelas develops from epidermal penetration of the pathogenic bacteria.
Group A Streptococcal Infection
- Group A streptococcal infection causes Erysipelas upon infiltration of the epidermis through a skin abrasion or lesion.[1]
- The streptococcal 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.
- Streptococcus pyogenes adheres to the dermis due to the following virulence factors:
- Containing M protein, allowing colonization.[2]
- Lipotechoic acid (LTA):
References
- ↑ Cunningham, M. W. (2000). "Pathogenesis of Group A Streptococcal Infections". Clinical Microbiology Reviews. 13 (3): 470–511. doi:10.1128/CMR.13.3.470-511.2000. ISSN 0893-8512.
- ↑ Ellen RP, Gibbons RJ (1972). "M protein-associated adherence of Streptococcus pyogenes to epithelial surfaces: prerequisite for virulence". Infect. Immun. 5 (5): 826–30. PMC 422446. PMID 4564883.