Strep throat pathophysiology: Difference between revisions
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==Overview== | ==Overview== | ||
[[Group A streptococcal pharyngitis|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 [[Adhesin|adhesins]] on the surface of organism. It then invades the [[Mucosal|mucosal tissue]] by producing various [[proteases]] and cytolysins causing [[inflammation]], which manifests as the signs and symptoms of pharyngitis.<ref name="cdcp">http://www.cdc.gov/groupastrep/diseases-hcp/strep-throat.html Accessed on October 18, 2016</ref><ref name="pmid10885988">{{cite journal| author=Cunningham MW| title=Pathogenesis of group A streptococcal infections. | journal=Clin Microbiol Rev | year= 2000 | volume= 13 | issue= 3 | pages= 470-511 | pmid=10885988 | doi= | pmc=88944 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10885988 }} </ref> | [[Group A streptococcal pharyngitis|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 [[Adhesin|adhesins]] on the surface of organism. It then invades the [[Mucosal|mucosal tissue]] by producing various [[proteases]] and [[Cytolysin|cytolysins]] causing [[inflammation]], which manifests as the signs and symptoms of [[pharyngitis]].<ref name="cdcp">http://www.cdc.gov/groupastrep/diseases-hcp/strep-throat.html Accessed on October 18, 2016</ref><ref name="pmid10885988">{{cite journal| author=Cunningham MW| title=Pathogenesis of group A streptococcal infections. | journal=Clin Microbiol Rev | year= 2000 | volume= 13 | issue= 3 | pages= 470-511 | pmid=10885988 | doi= | pmc=88944 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10885988 }} </ref> | ||
==Pathophysiology== | ==Pathophysiology== | ||
Pathophysiology of GAS throat infection may be described in the following steps:<ref name="cdcp">http://www.cdc.gov/groupastrep/diseases-hcp/strep-throat.html Accessed on October 18, 2016</ref><ref name="pmid10885988">{{cite journal| author=Cunningham MW| title=Pathogenesis of group A streptococcal infections. | journal=Clin Microbiol Rev | year= 2000 | volume= 13 | issue= 3 | pages= 470-511 | pmid=10885988 | doi= | pmc=88944 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10885988 }} </ref><ref name="pmid22642914">{{cite journal| author=Henningham A, Barnett TC, Maamary PG, Walker MJ| title=Pathogenesis of group A streptococcal infections. | journal=Discov Med | year= 2012 | volume= 13 | issue= 72 | pages= 329-42 | pmid=22642914 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22642914 }} </ref><ref name="pmid20353302">{{cite journal| author=Bessen DE, Lizano S| title=Tissue tropisms in group A streptococcal infections. | journal=Future Microbiol | year= 2010 | volume= 5 | issue= 4 | pages= 623-38 | pmid=20353302 | doi=10.2217/fmb.10.28 | pmc=2901552 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20353302 }} </ref><ref name="pmid19721085">{{cite journal| author=Nobbs AH, Lamont RJ, Jenkinson HF| title=Streptococcus adherence and colonization. | journal=Microbiol Mol Biol Rev | year= 2009 | volume= 73 | issue= 3 | pages= 407-50, Table of Contents | pmid=19721085 | doi=10.1128/MMBR.00014-09 | pmc=2738137 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19721085 }} </ref> | Pathophysiology of GAS throat infection may be described in the following steps:<ref name="cdcp">http://www.cdc.gov/groupastrep/diseases-hcp/strep-throat.html Accessed on October 18, 2016</ref><ref name="pmid10885988">{{cite journal| author=Cunningham MW| title=Pathogenesis of group A streptococcal infections. | journal=Clin Microbiol Rev | year= 2000 | volume= 13 | issue= 3 | pages= 470-511 | pmid=10885988 | doi= | pmc=88944 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10885988 }} </ref><ref name="pmid22642914">{{cite journal| author=Henningham A, Barnett TC, Maamary PG, Walker MJ| title=Pathogenesis of group A streptococcal infections. | journal=Discov Med | year= 2012 | volume= 13 | issue= 72 | pages= 329-42 | pmid=22642914 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22642914 }} </ref><ref name="pmid20353302">{{cite journal| author=Bessen DE, Lizano S| title=Tissue tropisms in group A streptococcal infections. | journal=Future Microbiol | year= 2010 | volume= 5 | issue= 4 | pages= 623-38 | pmid=20353302 | doi=10.2217/fmb.10.28 | pmc=2901552 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20353302 }} </ref><ref name="pmid19721085">{{cite journal| author=Nobbs AH, Lamont RJ, Jenkinson HF| title=Streptococcus adherence and colonization. | journal=Microbiol Mol Biol Rev | year= 2009 | volume= 73 | issue= 3 | pages= 407-50, Table of Contents | pmid=19721085 | doi=10.1128/MMBR.00014-09 | pmc=2738137 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19721085 }} </ref> | ||
===Transmission === | ===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.<ref name="cdcp">http://www.cdc.gov/groupastrep/diseases-hcp/strep-throat.html Accessed on October 18, 2016</ref> | [[Group A streptococci|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]].<ref name="cdcp">http://www.cdc.gov/groupastrep/diseases-hcp/strep-throat.html Accessed on October 18, 2016</ref> | ||
===Incubation period=== | ===Incubation period=== | ||
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===Pathogenesis=== | ===Pathogenesis=== | ||
The pathogenesis of GAS in the throat involves adhesion of bacteria to pharyngeal mucosa with the help of [[adhesin|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]].<ref name="pmid10885988">{{cite journal| author=Cunningham MW| title=Pathogenesis of group A streptococcal infections. | journal=Clin Microbiol Rev | year= 2000 | volume= 13 | issue= 3 | pages= 470-511 | pmid=10885988 | doi= | pmc=88944 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10885988 }} </ref> | |||
M protein on the surface of group A streptococcal infection plays important role in the pathogenesis of [[rheumatic fever]].<ref name="pmid17305559">{{cite journal| author=Guilherme L, Faé KC, Oshiro SE, Tanaka AC, Pomerantzeff PM, Kalil J| title=T cell response in rheumatic fever: crossreactivity between streptococcal M protein peptides and heart tissue proteins. | journal=Curr Protein Pept Sci | year= 2007 | volume= 8 | issue= 1 | pages= 39-44 | pmid=17305559 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17305559 }} </ref> | * The pathogenesis of GAS in the throat involves [[Adhesion|adhesion of bacteria]] to pharyngeal [[mucosa]] with the help of [[adhesin|adhesins]] on the surface of organism. | ||
* It then invades the mucosal tissue by producing various [[proteases]] and [[Cytolysin|cytolysins]] causing [[inflammation]] manifesting as signs and symptoms of [[pharyngitis]].<ref name="pmid10885988">{{cite journal| author=Cunningham MW| title=Pathogenesis of group A streptococcal infections. | journal=Clin Microbiol Rev | year= 2000 | volume= 13 | issue= 3 | pages= 470-511 | pmid=10885988 | doi= | pmc=88944 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10885988 }} </ref> | |||
* M protein on the surface of [[group A streptococcal infection]] plays important role in the pathogenesis of [[rheumatic fever]].<ref name="pmid17305559">{{cite journal| author=Guilherme L, Faé KC, Oshiro SE, Tanaka AC, Pomerantzeff PM, Kalil J| title=T cell response in rheumatic fever: crossreactivity between streptococcal M protein peptides and heart tissue proteins. | journal=Curr Protein Pept Sci | year= 2007 | volume= 8 | issue= 1 | pages= 39-44 | pmid=17305559 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17305559 }} </ref> | |||
==Genetic association== | ==Genetic association== | ||
*HLA-DRB1*07 allele may have a role in recurrent streptococcal pharyngitis and [[rheumatic heart disease]].<ref name="pmid17026463">{{cite journal| author=Haydardedeoğlu FE, Tutkak H, Köse K, Düzgün N| title=Genetic susceptibility to rheumatic heart disease and streptococcal pharyngitis: association with HLA-DR alleles. | journal=Tissue Antigens | year= 2006 | volume= 68 | issue= 4 | pages= 293-6 | pmid=17026463 | doi=10.1111/j.1399-0039.2006.00678.x | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17026463 }} </ref> | *HLA-DRB1*07 [[allele]] may have a role in recurrent streptococcal pharyngitis and [[rheumatic heart disease]].<ref name="pmid17026463">{{cite journal| author=Haydardedeoğlu FE, Tutkak H, Köse K, Düzgün N| title=Genetic susceptibility to rheumatic heart disease and streptococcal pharyngitis: association with HLA-DR alleles. | journal=Tissue Antigens | year= 2006 | volume= 68 | issue= 4 | pages= 293-6 | pmid=17026463 | doi=10.1111/j.1399-0039.2006.00678.x | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17026463 }} </ref> | ||
*HLA-DRB1*11 allele may have a protective role in [[rheumatic heart disease]].<ref name="pmid17026463">{{cite journal| author=Haydardedeoğlu FE, Tutkak H, Köse K, Düzgün N| title=Genetic susceptibility to rheumatic heart disease and streptococcal pharyngitis: association with HLA-DR alleles. | journal=Tissue Antigens | year= 2006 | volume= 68 | issue= 4 | pages= 293-6 | pmid=17026463 | doi=10.1111/j.1399-0039.2006.00678.x | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17026463 }} </ref> | *HLA-DRB1*11 [[allele]] may have a protective role in [[rheumatic heart disease]].<ref name="pmid17026463">{{cite journal| author=Haydardedeoğlu FE, Tutkak H, Köse K, Düzgün N| title=Genetic susceptibility to rheumatic heart disease and streptococcal pharyngitis: association with HLA-DR alleles. | journal=Tissue Antigens | year= 2006 | volume= 68 | issue= 4 | pages= 293-6 | pmid=17026463 | doi=10.1111/j.1399-0039.2006.00678.x | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17026463 }} </ref> | ||
==References== | ==References== | ||
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{{WH}} | {{WH}} | ||
{{WS}} | {{WS}} | ||
[[Category:Emergency mdicine]] | |||
[[Category:Disease]] | |||
[[Category:Up-To-Date]] | |||
[[Category:Infectious disease]] | |||
[[Category:Pediatrics]] | |||
[[Category:Otolaryngology]] | |||
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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. 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 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
- 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
- ↑ 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.