Talk:Streptococcus agalactiae

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Streptococcus Agalactiae
Scientific classification
Binomial name
Streptococcus Agalactiae

Description and significance

Streptococcus Agalactiae, also known as Group B streptococci are gram positive cocci that range from 0.6 to 1.2 um. These cocci arrange themselves in chains, forming shorter chains in clinical specimens and longer chains in a culture specimen. They are distinguished from other streptococci by the presence of the group B antigen.

S. agalactiae colonizes in a woman’s vaginal and gastrointestinal tracts in a commensal relationship that is present in 25-40% of healthy women. When the organism is introduced to a weakened or susceptible host (including individuals with compromised immunity and newborns), S. Agalactiae causes bacterial sepsis, pneumonia and meningitis in newborns and can also cause postpartum infection, neonatal sepsis and other infections in infected hosts.

Cell structure and metabolism

S. agalactiae are facultative anerobes that are both B-hemoltyic and non hemolytic (hemolysis is the breakdown of red blood cells before the natural course of the red blood cell’s life). <ref>Medline Plus. 20 April 2002 http://www.nlm.nih.gov/medlineplus/ency/article/002372.htm/ref>

Different strains of streptococcus agalactiae have been identified by serologic markers that have classified different groups based on the prescence of either a B antigen or group specific cell wall polysaccharide antigen, a type-specific capsular polysaccharides or the presence of the surface (C) protein. The type-specific capsular polysaccharides have been lableled Ia, Ia/c, Ib/c, II, IIc, III, IV, V, VI, VII, VIII and are used as epidemiologic markers.

The cell structure of S. agalactiae helps to contribute to the organism’s virulence in several different ways. S. agalactiae contains a thick peptidoglycan cell wall layer which prevents dessication and allows for the organism to live on dry surfaces. The capsular polysaccharides Ia, III and V further contribute to the organism’s virulence by preventing the immune response of complement mediated phagocytosis. In addition, the organism’s virulence is heightened by the presence of hydrolytic enzymes that aide in the spread of bacteria and allow for host tissue destruction.