Group B streptococcal infection pathophysiology: Difference between revisions
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* [[Respiratory tract]] | * [[Respiratory tract]] | ||
The series of events that explain the pathophysiology of GBS infection can be summarized as follows: | The series of events that explain the pathophysiology of GBS infection can be summarized as follows:<ref name="pmid15458402">{{cite journal| author=Doran KS, Nizet V| title=Molecular pathogenesis of neonatal group B streptococcal infection: no longer in its infancy. | journal=Mol Microbiol | year= 2004 | volume= 54 | issue= 1 | pages= 23-31 | pmid=15458402 | doi=10.1111/j.1365-2958.2004.04266.x | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15458402 }} </ref> | ||
* [[Extracellular matrix]] binding | * [[Extracellular matrix]] binding | ||
* Direct cellular injury | * Direct cellular injury | ||
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===Virulence Factors=== | ===Virulence Factors=== | ||
The polysaccharide antiphagocytic capsule is this bacterium's main [[virulence factor]]. | The polysaccharide antiphagocytic capsule is this bacterium's main [[virulence factor]].<ref name="pmid15458402">{{cite journal| author=Doran KS, Nizet V| title=Molecular pathogenesis of neonatal group B streptococcal infection: no longer in its infancy. | journal=Mol Microbiol | year= 2004 | volume= 54 | issue= 1 | pages= 23-31 | pmid=15458402 | doi=10.1111/j.1365-2958.2004.04266.x | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15458402 }} </ref> | ||
Other key virulence factors include: | Other key virulence factors include: | ||
* Beta-hemolysin | * Beta-hemolysin | ||
* | * C protein | ||
* C5a peptidase | * C5a peptidase | ||
* [[CAMP]] factor | * [[CAMP]] factor | ||
* [[Fibrinogen | * [[Fibrinogen]] receptor | ||
* [[Hyaluronate lyase]] | * [[Hyaluronate lyase]] | ||
* | * Lipotechoic acid | ||
* [[Serine protease]] | * [[Serine protease]] | ||
Revision as of 14:06, 21 August 2014
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Group B Streptococcal Infection Microchapters |
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Differentiating Group B Streptococcal Infection from other Diseases |
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Diagnosis |
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Group B streptococcal infection pathophysiology On the Web |
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Risk calculators and risk factors for Group B streptococcal infection pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Rim Halaby, M.D. [2]
Overview
Pathophysiology
Pathogenesis
GBS is characterized by its ability to adhere to epithelial surfaces, particularly the vaginal mucosa where the pH is low. The types of epithelium to which GBS adheres to are:
- Vagina
- Placental membranes
- Blood brain barrier
- Respiratory tract
The series of events that explain the pathophysiology of GBS infection can be summarized as follows:[1]
- Extracellular matrix binding
- Direct cellular injury
- Invasion of epithelial cells and brain endothelium
- Resistance to intracellular killing
- Resistance to phagocytosis
- Activation of inflamamtory cells
- Recruitment of neutrophils in the central nervous system
Virulence Factors
The polysaccharide antiphagocytic capsule is this bacterium's main virulence factor.[1]
Other key virulence factors include:
- Beta-hemolysin
- C protein
- C5a peptidase
- CAMP factor
- Fibrinogen receptor
- Hyaluronate lyase
- Lipotechoic acid
- Serine protease
Transmission
GBS in Pregnancy
The gastrointestinal tract serves as the primary reservoir for GBS and is the likely source of vaginal colonization.
GBS in Neonates
Early-onset infections are acquired vertically through exposure to GBS from the vagina of a colonized woman. Neonatal infection occurs primarily when GBS ascends from the vagina to the amniotic fluid after onset of labor or rupture of membranes, although GBS also can invade through intact membranes. GBS can be aspirated into the fetal lungs, which in turn can lead to bacteremia. Infants also can become infected with GBS during passage through the birth canal; infants who are exposed to the organism through this route can become colonized at mucus membrane sites in the gastrointestinal or respiratory tracts, but these colonized infants most commonly remain healthy.
References
- ↑ 1.0 1.1 Doran KS, Nizet V (2004). "Molecular pathogenesis of neonatal group B streptococcal infection: no longer in its infancy". Mol Microbiol. 54 (1): 23–31. doi:10.1111/j.1365-2958.2004.04266.x. PMID 15458402.