Sandbox: GAS pathophysiology: Difference between revisions
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*The affected tissue of patients with severe cases of [[necrotizing fasciitis]] are devoid of [[neutrophil]]s.<ref name=Hidalgo-Grass_2004>{{cite journal |author=Hidalgo-Grass C, Dan-Goor M, Maly A, Eran Y, Kwinn L, Nizet V, Ravins M, Jaffe J, Peyser A, Moses A, Hanski E |title=Effect of a bacterial pheromone peptide on host chemokine degradation in group A streptococcal necrotising soft-tissue infections |journal=Lancet |volume=363 |issue=9410 |pages=696-703 |year=2004 |id=PMID 15001327}}</ref>. The [[serine protease]] ScpC, which is released by ''S. pyogenes'', is responsible for preventing the migration of neutrophils to the spreading infection.<ref name="Hidalgo-Grass 2006">{{cite journal |author=Hidalgo-Grass C, Mishalian I, Dan-Goor M, Belotserkovsky I, Eran Y, Nizet V, Peled A, Hanski E |title=A streptococcal protease that degrades CXC chemokines and impairs bacterial clearance from infected tissues |journal=EMBO J |volume=25 |issue=19 |pages=4628-37 |year=2006 |id=PMID 16977314}}</ref> ScpC degrades the [[chemokine]] [[IL-8]], which would otherwise attract [[neutrophil]]s to the site of infection. C5a peptidase, although required to degrade the neutrophil chemotaxin C5a in the early stages of infection, is not required for ''S. pyogenes'' to prevent the influx of neutrophils as the bacteria spread through the [[fascia]].<ref name="Ji 1996"/><ref name="Hidalgo-Grass 2006"/> | *The affected tissue of patients with severe cases of [[necrotizing fasciitis]] are devoid of [[neutrophil]]s.<ref name=Hidalgo-Grass_2004>{{cite journal |author=Hidalgo-Grass C, Dan-Goor M, Maly A, Eran Y, Kwinn L, Nizet V, Ravins M, Jaffe J, Peyser A, Moses A, Hanski E |title=Effect of a bacterial pheromone peptide on host chemokine degradation in group A streptococcal necrotising soft-tissue infections |journal=Lancet |volume=363 |issue=9410 |pages=696-703 |year=2004 |id=PMID 15001327}}</ref>. The [[serine protease]] ScpC, which is released by ''S. pyogenes'', is responsible for preventing the migration of neutrophils to the spreading infection.<ref name="Hidalgo-Grass 2006">{{cite journal |author=Hidalgo-Grass C, Mishalian I, Dan-Goor M, Belotserkovsky I, Eran Y, Nizet V, Peled A, Hanski E |title=A streptococcal protease that degrades CXC chemokines and impairs bacterial clearance from infected tissues |journal=EMBO J |volume=25 |issue=19 |pages=4628-37 |year=2006 |id=PMID 16977314}}</ref> ScpC degrades the [[chemokine]] [[IL-8]], which would otherwise attract [[neutrophil]]s to the site of infection. C5a peptidase, although required to degrade the neutrophil chemotaxin C5a in the early stages of infection, is not required for ''S. pyogenes'' to prevent the influx of neutrophils as the bacteria spread through the [[fascia]].<ref name="Ji 1996"/><ref name="Hidalgo-Grass 2006"/> | ||
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==References== | ==References== | ||
{{Reflist|2}} | {{Reflist|2}} |
Revision as of 21:42, 29 May 2017
Transmission
Group A streptococcal infection can be transmitted by the following:[1]
- Direct inter-personal transmission
- Infected airborne droplets
Virulence factors
Group A streptococcus are responsible for various diseases ranging from mild to life threatening cases. The bacteria depends mainly on many virulence factors which are responsible for the pathogenesis of the infections.[1]
Virulence factors | Mechanism of action |
---|---|
M - protein |
|
Streptolysin O and S |
|
Streptococcal pyrogenic exotoxins A and C |
|
Streptokinase |
|
Hyalourinidase |
|
Streptodornase |
|
C5a peptidase |
|
Streptococcal chemokine protease |
|
References
- ↑ 1.0 1.1 Brouwer S, Barnett TC, Rivera-Hernandez T, Rohde M, Walker MJ (2016). "Streptococcus pyogenes adhesion and colonization". FEBS Lett. 590 (21): 3739–3757. doi:10.1002/1873-3468.12254. PMID 27312939.
- ↑ Starr C, Engleberg N (2006). "Role of hyaluronidase in subcutaneous spread and growth of group A streptococcus". Infect Immun. 74 (1): 40–8. PMID 16368955.
- ↑ Buchanan J, Simpson A, Aziz R, Liu G, Kristian S, Kotb M, Feramisco J, Nizet V (2006). "DNase expression allows the pathogen group A Streptococcus to escape killing in neutrophil extracellular traps". Curr Biol. 16 (4): 396–400. PMID 16488874.
- ↑ Wexler D, Chenoweth D, Cleary P (1985). "Mechanism of action of the group A streptococcal C5a inactivator". Proc Natl Acad Sci U S A. 82 (23): 8144–8. PMID 3906656.
- ↑ 5.0 5.1 Ji Y, McLandsborough L, Kondagunta A, Cleary P (1996). "C5a peptidase alters clearance and trafficking of group A streptococci by infected mice". Infect Immun. 64 (2): 503–10. PMID 8550199.
- ↑ Hidalgo-Grass C, Dan-Goor M, Maly A, Eran Y, Kwinn L, Nizet V, Ravins M, Jaffe J, Peyser A, Moses A, Hanski E (2004). "Effect of a bacterial pheromone peptide on host chemokine degradation in group A streptococcal necrotising soft-tissue infections". Lancet. 363 (9410): 696–703. PMID 15001327.
- ↑ 7.0 7.1 Hidalgo-Grass C, Mishalian I, Dan-Goor M, Belotserkovsky I, Eran Y, Nizet V, Peled A, Hanski E (2006). "A streptococcal protease that degrades CXC chemokines and impairs bacterial clearance from infected tissues". EMBO J. 25 (19): 4628–37. PMID 16977314.