Group B streptococcal infection pathophysiology: Difference between revisions

Jump to navigation Jump to search
VisualWikitext
No edit summary
m (Changes made per Mahshid's request)
 
(10 intermediate revisions by one other user not shown)
Line 4: Line 4:


==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==
===Virulence Factor===
 
The polysaccharide antiphagocytic capsule is this bacterium's main [[virulence factor]].  
===Pathogenesis===
GBS is characterized by its ability to adhere to [[epithelial]] surfaces, particularly the [[vagina|vaginal]] mucosa where the pH is low.  The types of epithelium to which GBS adheres to are:
* [[Vagina]]
* [[Placenta]]l membranes
* [[Blood brain barrier]]
* [[Respiratory tract]]
 
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>
* [[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 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.
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==
Line 23: Line 52:
[[Category:Streptococcaceae]]
[[Category:Streptococcaceae]]
[[Category:Obstetrics]]
[[Category:Obstetrics]]
[[Category:Infectious disease]]
 
[[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

Group B Streptococcal Infection Microchapters

Home

Patient Information

Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differentiating Group B Streptococcal Infection from other Diseases

Epidemiology and Demographics

Risk Factors

Screening

Natural History, Complications and Prognosis

Diagnosis

History and Symptoms

Physical Examination

Laboratory Findings

Treatment

Medical Therapy

Primary Prevention

Secondary Prevention

Future or Investigational Therapies

Case Studies

Case #1

Group B streptococcal infection pathophysiology On the Web

Most recent articles

Most cited articles

Review articles

CME Programs

Powerpoint slides

Images

American Roentgen Ray Society Images of Group B streptococcal infection pathophysiology

All Images
X-rays
Echo & Ultrasound
CT Images
MRI

Ongoing Trials at Clinical Trials.gov

US National Guidelines Clearinghouse

NICE Guidance

FDA on Group B streptococcal infection pathophysiology

CDC on Group B streptococcal infection pathophysiology

Group B streptococcal infection pathophysiology in the news

Blogs on Group B streptococcal infection pathophysiology

Directions to Hospitals Treating Group B streptococcal infection

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

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:

The series of events that explain the pathogenesis of GBS infection can be summarized as follows:[1]

Virulence Factors

The polysaccharide antiphagocytic capsule is this bacterium's main virulence factor.

Other key virulence factors include:[1]

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. ↑ 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. ↑ 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

Template:Bacterial diseases


Template:WikiDoc Sources

Retrieved from "https://www.wikidoc.org/index.php?title=Group_B_streptococcal_infection_pathophysiology&oldid=1355929"