Strep throat pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Aysha Anwar, M.B.B.S[2]
Overview
Group A strep pharyngitis is most commonly spread through direct person-to-person transmission, typically through saliva or nasal secretions from an infected person. Rarely, contaminated food, especially milk and milk products, can result in outbreaks.The incubation period of group A strep pharyngitis is approximately 2 to 5 days. Pathogenesis of GAS throat involves adhesion of bacteria to pharyngeal mucosa with the help of adhesins on the surface of organism. It then invades the mucosal tissue by producing various proteases and cytolysins causing inflammation manifesting as signs and symptoms of pharyngitis.[1][2]
Pathophysiology
Pathophysiology of GAS throat infection may be described in the following steps:
Transmission
Group A strep pharyngitis is most commonly spread through direct person-to-person transmission, typically through saliva or nasal secretions from an infected person. Rarely, contaminated food, especially milk and milk products, can result in outbreaks.[1]
Incubation period
The incubation period of group A strep pharyngitis is approximately 2 to 5 days.[1]
Pathogenesis
Pathogenesis of GAS throat involves adhesion of bacteria to pharyngeal mucosa with the help of adhesins on the surface of organism. It then invades the mucosal tissue by producing various proteases and cytolysins causing inflammation manifesting as signs and symptoms of pharyngitis.[2] M protein on the surface of group A streptococcal infection plays important role in the pathogenesis of rheumatic fever.