Impetigo pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
The infection is spread by direct contact with lesions or with nasal carriers. The incubation period is 1–3 days. Dried streptococci in the air are not infectious to intact skin. Scratching may spread the lesions.
Pathogenesis
- Impetigo, the infection of epidermis, can either be primary or secondary to scratches, injuries, bites or conditions that lead to a break in the continuity of the skin. The breaks in the continuity are potential sites for the pathogens to enter and infect.[1]
- The D and E strains of emm protein act as a virulence factor for group A Streptococci.[1][2]
Bullous Impetigo
The following are important aspects in the pathophysiology of bullous impetigo:[3][4]
- Bullous impetigo is caused by exfoliative toxins which are released by Stapphylococcus aureus.
- The toxins are of two types, A and B, and lead to the production of bullae in the superficial layer of epidermis.
- These bullae are flaccid and can rupture easily.
Genetics
Associated Conditions
Gross Pathology
Microscopic Pathology
References
- ↑ 1.0 1.1 Wasserzug O, Valinsky L, Klement E, Bar-Zeev Y, Davidovitch N, Orr N; et al. (2009). "A cluster of ecthyma outbreaks caused by a single clone of invasive and highly infective Streptococcus pyogenes". Clin Infect Dis. 48 (9): 1213–9. doi:10.1086/597770. PMID 19331587.
- ↑ Bessen DE, Sotir CM, Readdy TL, Hollingshead SK (1996). "Genetic correlates of throat and skin isolates of group A streptococci". J Infect Dis. 173 (4): 896–900. PMID 8603968.
- ↑ Cohen PR (2016). "Bullous impetigo and pregnancy: Case report and review of blistering conditions in pregnancy". Dermatol Online J. 22 (4). PMID 27617460.
- ↑ Duggal SD, Bharara T, Jena PP, Kumar A, Sharma A, Gur R; et al. (2016). "Staphylococcal bullous impetigo in a neonate". World J Clin Cases. 4 (7): 191–4. doi:10.12998/wjcc.v4.i7.191. PMC 4945591. PMID 27458596.