Group B streptococcal infection pathophysiology: Difference between revisions
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==Overview== | ==Overview== | ||
The [[gastrointestinal tract]] serves as the primary reservoir for Group B Streptococcus (GBS) and is the likely source of [[vagina]]l colonization. Early-onset neonatal infections are acquired vertically through exposure to GBS from the [[vagina]] of a colonized woman. GBS is characterized by its ability to adhere to [[epithelial]] surfaces, such as the [[vagina]], [[placenta]]l membranes, [[blood brain barrier]], and [[respiratory tract]]. GBS can penetrate the host cell barriers and evade the host's [[immune response]]. The polysaccharide antiphagocytic capsule is this bacterium's main [[virulence factor]]. | |||
==Pathophysiology== | ==Pathophysiology== | ||
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* [[Respiratory tract]] | * [[Respiratory tract]] | ||
===Virulence | The series of events that explain the pathogenesis 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> | ||
The polysaccharide antiphagocytic capsule is this bacterium's main [[virulence factor]]. | * [[Extracellular matrix]] binding | ||
* Direct cellular injury | |||
* Invasion of [[epithelial cell]]s and brain [[endothelium]] | |||
* Resistance to intracellular killing | |||
* Resistance to [[phagocytosis]] | |||
* Activation of [[inflammatory cell]]s | |||
* Recruitment of [[neutrophil]]s in the [[central nervous system]] | |||
===Virulence Factors=== | |||
The polysaccharide antiphagocytic capsule is this bacterium's main [[virulence factor]]. | |||
Other key virulence factors include:<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> | |||
* Beta-hemolysin | |||
* C protein | |||
* C5a peptidase | |||
* [[CAMP]] factor | |||
* [[Fibrinogen]] receptor | |||
* [[Hyaluronate lyase]] | |||
* Lipotechoic acid | |||
* [[Serine protease]] | |||
===Transmission=== | ===Transmission=== | ||
====GBS in Pregnancy==== | ====GBS in Pregnancy==== | ||
The gastrointestinal tract serves as the primary reservoir for GBS and is the likely source of vaginal colonization. | The [[gastrointestinal tract]] serves as the primary reservoir for GBS and is the likely source of vaginal colonization.<ref name=CDCMMWR>Verani J.R., McGee L, and Schrag S.J. Prevention of Perinatal Group B Streptococcal Disease. Revised Guidelines from CDC, 2010.[http://www.cdc.gov/mmwr/preview/mmwrhtml/rr5910a1.htm?s_cid=rr5910a1_w CDC.gov]</ref> | ||
====GBS in Neonates==== | ====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 | 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 [[lung]]s, 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 tract|gastrointestinal]] or [[respiratory tract]]s, but these colonized infants most commonly remain healthy.<ref name=CDCMMWR>Verani J.R., McGee L, and Schrag S.J. Prevention of Perinatal Group B Streptococcal Disease. Revised Guidelines from CDC, 2010.[http://www.cdc.gov/mmwr/preview/mmwrhtml/rr5910a1.htm?s_cid=rr5910a1_w CDC.gov]</ref> | ||
==References== | ==References== | ||
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[[Category:Streptococcaceae]] | [[Category:Streptococcaceae]] | ||
[[Category:Obstetrics]] | [[Category:Obstetrics]] | ||
[[Category:Mature chapter]] | [[Category:Mature chapter]] | ||
[[Category:Pediatrics]] | |||
[[Category:Neonatology]] | |||
{{WikiDoc Help Menu}} | {{WikiDoc Help Menu}} | ||
{{WikiDoc Sources}} | {{WikiDoc Sources}} | ||
Latest revision as of 17:51, 18 September 2017
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Group B Streptococcal Infection Microchapters |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Rim Halaby, M.D. [2]
Overview
The gastrointestinal tract serves as the primary reservoir for Group B Streptococcus (GBS) and is the likely source of vaginal colonization. Early-onset neonatal infections are acquired vertically through exposure to GBS from the vagina of a colonized woman. GBS is characterized by its ability to adhere to epithelial surfaces, such as the vagina, placental membranes, blood brain barrier, and respiratory tract. GBS can penetrate the host cell barriers and evade the host's immune response. The polysaccharide antiphagocytic capsule is this bacterium's main virulence factor.
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 pathogenesis 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 inflammatory cells
- Recruitment of neutrophils in the central nervous system
Virulence Factors
The polysaccharide antiphagocytic capsule is this bacterium's main virulence factor.
Other key virulence factors include:[1]
- 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.[2]
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.[2]
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.
- ↑ 2.0 2.1 Verani J.R., McGee L, and Schrag S.J. Prevention of Perinatal Group B Streptococcal Disease. Revised Guidelines from CDC, 2010.CDC.gov