Query: NC_009009:1876367 Streptococcus sanguinis SK36, complete genome Lineage: Streptococcus sanguinis; Streptococcus; Streptococcaceae; Lactobacillales; Firmicutes; Bacteria General Information: This strain was isolated from human dental plaque in 1980 and is virulent in a rat model. Indigenous oral bacteria that causes dental decay and possibly endocarditis. Most streptococci are facultative anaerobes, and some are obligate anaerobes. Serologic grouping is based on antigenic differences in cell wall carbohydrates, in cell wall pili-associated protein, and in the polysaccharide capsule in group B streptococci. This microbe is found associated with human oral bacterial communities and can colonize the dental surfaces, aiding other organisms in attachment. Progression of caries and periodontal disease are associated with this microbe as is endocarditis which can lead to death.
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General Information: This well studied laboratory strain (Porton isolate) is not virulent due to the loss of the two plasmids, pXO1 and pXO2. Under starvation conditions this group of bacteria initiate a pathway that leads to endospore formation, a process that is thoroughly studied and is a model system for prokaryotic development and differentiation. Spores are highly resistant to heat, cold, dessication, radiation, and disinfectants, and enable the organism to persist in otherwise inhospitable environments. Under more inviting conditions the spores germinate to produce vegetative cells. This organism was the first to be shown to cause disease by Dr. Louis Pasteur (the organism, isolated from sick animals, was grown in the laboratory and then used to infect healthy animals and make them sick). This organism was also the first for which an attenuated strain was developed as a vaccine. Herbivorous animals become infected with the organism when they ingest spores from the soil whereas humans become infected when they come into contact with a contaminated animal. PA/LF and PA/EF complexes are internalized by host cells where the LF (metalloprotease) and EF (calmodulin-dependent adenylate cyclase) components act. At high levels LF induces cell death and release of the bacterium while EF increases host susceptibility to infection and promotes fluid accumulation in the cells.