Talk:Streptococcus agalactiae

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Streptococcus Agalactiae
Scientific classification
Kingdom: Bacteria Phylum: Firmicutes Class: Bacilli Order: Lactobacillales Family: Streptococcaceae Genus: Streptococcus Species: Streptococcus agalactiae
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).

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.

Genome structure

As there are several isolates of S. agalactiae, the genome sequence of different isolates have been determined and comparatively analyzed with other S. agalactiae strains. The study found that the circular S. agalactiae genome consists of 2,160,267 base pairs, including a G + C content of 35.7%, 80 tRNAs, 7 rRNAs and 3 sRNAs. The project predicted that the genome encodes for 2,175 proteins, 61% of which (1,333) were identified, while the remaining proteins coded by the genome are “of unknown function.”

In addition, the genome sequencing experiment identified various genes that act as possible virulence factors. Several genes such as Sip (SAG0032), CAMP factor (SAG2043), R5 protein (SAG1331), Streptococcal enolase (SAG0628), hyaluronidase (SAG1197) and hemolysin/cytolysin (cylE, SAG0669), have been identified as coding for surface proteins or secretory proteins that contribute to the organisms virulence or aide in the organism’s immunity against host defenses.

The genome project highlighted the unique membrane structure of S. agalactiae as it identified the S. agalactiae genomic sequences that code for the B antigen present on the surface of all S. agalactiae strains and the capsular polysaccharide specific to each strain of S. agalactiae. The project also recognized nine differing capsular polysaccharides types, each one containing salic acid structures. These units are part of a repeating structure that prevent the activation of the host’s alternative complement pathway and thereby contribute to the organism’s virulence.

The sequencing project also undertook comparative genomics, comparing the genome of S. agalactiae to that of its common streptococci, S. pneumoniae and S. pyogenes. The analysis discovered 1,060 homologous genes in the three genomes and identified 683 genes specific to S. agalactiae only. These findings are in line with the relationships between the different strains, which must have similar gene factors as they all cause invasive diseases, but cannot have identical genomes as they each colonize and invade different areas and cause different diseases. For example, while S. agalactiae codes for the synthesis of arginine, asparate and citruline, it is missing the genes that S. pneumoniae and S. pyogenes use to synthesize fucose, lactose, mannitol, raffinose, lysine, and threonine. The differining genes are most probably a reflection of the differening hosts between the organisms.

While there are various different serotypes of S. agalactiae, the genomic variations between and within serotypes are not well recognized. It has been hypothesized, however, that these variations are mainly unique to S. Agalactiae, as while 260 (38%) of S. agalactiae’s unique 683 genes vary amongst different S. agalactiae serotypes, only 47 (4%) of the genes found in all three streptococci strains vary amongst different S. agalactiae serotypes.