Strep throat pathophysiology
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aysha Anwar, M.B.B.S[2]
Overview
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. The 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, which manifests as the signs and symptoms of pharyngitis.[1][2]
Pathophysiology
Pathophysiology
Pathophysiology of GAS throat infection may be described in the following steps:[1][2][3][4][5]
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
- The pathogenesis of GAS in the 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.[6]
Genetic association
Genetic association
- HLA-DRB1*07 allele may have a role in recurrent streptococcal pharyngitis and rheumatic heart disease.[7]
- HLA-DRB1*11 allele may have a protective role in rheumatic heart disease.[7]
References
References
- ↑ 1.0 1.1 1.2 1.3 http://www.cdc.gov/groupastrep/diseases-hcp/strep-throat.html Accessed on October 18, 2016
- ↑ 2.0 2.1 2.2 Cunningham MW (2000). “Pathogenesis of group A streptococcal infections”. Clin Microbiol Rev. 13 (3): 470–511. PMC 88944. PMID 10885988.
- ↑ Henningham A, Barnett TC, Maamary PG, Walker MJ (2012). “Pathogenesis of group A streptococcal infections”. Discov Med. 13 (72): 329–42. PMID 22642914.
- ↑ Bessen DE, Lizano S (2010). “Tissue tropisms in group A streptococcal infections”. Future Microbiol. 5 (4): 623–38. doi:10.2217/fmb.10.28. PMC 2901552. PMID 20353302.
- ↑ Nobbs AH, Lamont RJ, Jenkinson HF (2009). “Streptococcus adherence and colonization”. Microbiol Mol Biol Rev. 73 (3): 407–50, Table of Contents. doi:10.1128/MMBR.00014-09. PMC 2738137. PMID 19721085.
- ↑ Guilherme L, Faé KC, Oshiro SE, Tanaka AC, Pomerantzeff PM, Kalil J (2007). “T cell response in rheumatic fever: crossreactivity between streptococcal M protein peptides and heart tissue proteins”. Curr Protein Pept Sci. 8 (1): 39–44. PMID 17305559.
- ↑ 7.0 7.1 Haydardedeoğlu FE, Tutkak H, Köse K, Düzgün N (2006). “Genetic susceptibility to rheumatic heart disease and streptococcal pharyngitis: association with HLA-DR alleles”. Tissue Antigens. 68 (4): 293–6. doi:10.1111/j.1399-0039.2006.00678.x. PMID 17026463.
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