VIOLIN Logo
VO Banner
Search: for Help
About
Introduction
Statistics
VIOLIN News
Your VIOLIN
Register or Login
Submission
Tutorial
Vaccine & Components
Vaxquery
Vaxgen
VBLAST
Protegen
VirmugenDB
DNAVaxDB
CanVaxKB
Vaxjo
Vaxvec
Vevax
Huvax
Cov19VaxKB
Host Responses
VaximmutorDB
VIGET
Vaxafe
Vaxar
Vaxism
Vaccine Literature
VO-SciMiner
Litesearch
Vaxmesh
Vaxlert
Vaccine Design
Vaxign2
Vaxign
Community Efforts
Vaccine Ontology
ICoVax 2012
ICoVax 2013
Advisory Committee
Vaccine Society
Vaxperts
VaxPub
VaxCom
VaxLaw
VaxMedia
VaxMeet
VaxFund
VaxCareer
Data Exchange
V-Utilities
VIOLINML
Help & Documents
Publications
Documents
FAQs
Links
Acknowledgements
Disclaimer
Contact Us
UM Logo

Pathogen Page
Streptococcus agalactiae
I. General Information
1. NCBI Taxonomy ID:
1311
2. Disease:
Group B streptococcus (GBS) infection
3. Introduction
S. agalactiae is a member of the gastrointestinal normal flora in some humans and can spread to secondary sites - including the vagina in 10-30% of women. This is of clinical importance: S. agalactiae can be transferred to a neonate passing through the birth canal and can cause serious group B streptococcal infection. In the western world, S. agalactiae is the main cause of bacterial septicemia of the newborn, which can lead to death or long-term sequelae. S. agalactiae invade via alveolar and pulmonary epithelial cells; newborns are especially succeptible to infection because they lack alveolar macrophages to prevent invasion. Newborn GBS disease is separated into early-onset disease occurring on living days 0-7 and late-onset disease which starts on days 7-90. Early-onset septicemia is more prone to be accompanied by pneumonia, while late-onset septicimia is more often accompanied by meningitis. S. agalactiae neonatal meningitis does often not present with the hallmark sign of adult meningitis, a stiff neck; rather, it presents with nonspecific symptoms such as fever, vomiting and irritability and can consequently lead to late diagnosis. Hearing loss can be a long-term sequelae of GBS-meningitis. Infection with GBS is the cause of some instances of stillbirth (Wiki: S. agalactiae).
4. Microbial Pathogenesis
Experimental study of early-onset infection suggests that this bacteria to invade fetal epithelial and endothelial cells and certain macrophages and the mortality rates for early-onset is 4-6%. This invasion is confirmed to play important role in its pathogenesis through the ability of S. agalactiae in the monkey model. Ability to invade and transcytose, this bacteria can enter into the respiratory tract causing pneumonia or further into the blood causing septicemia. Bloodstream enables this bacteria to reach different sites of body causing meningitis and osteomyelitis (MicrobeWiki: S. agalactiae).
5. Host Ranges and Animal Models
S. agalactiae colonizes in the body of some animals, including cow, sheep, and humans without causing any harm. The habitat of this microorganism is largely confined to the intestine and vagina in human and the mammary gland of cows and sheep. This microorganism also colonizes in the genital and/or intestinal tract of about 10-30% of pregnant women. However, some can actually cause diseases in their neonates or immunocompromised mammals. Monkeys and mice can be used as a model of disease (MicrobeWiki: S. agalactiae).
6. Host Protective Immunity
Passive immunization with antibodies has been shown to be protective in mice (Erdogan et al., 2002).
Loading...
Loading Pathogen Genes...
Loading...
Loading Host Genes...
Loading...
Loading Vaccines...
Loading References...