Query: NC_016513:1126263 Aggregatibacter actinomycetemcomitans ANH9381 chromosome, complete Lineage: Aggregatibacter actinomycetemcomitans; Aggregatibacter; Pasteurellaceae; Pasteurellales; Proteobacteria; Bacteria General Information: Aggregatibacter actinomycetemcomitans, previously Actinobacillus actinomycetemcomitans typically resides in the oral cavity of humans and animals and can cause a number of diseases. The bacterium, along with 3 other organisms, is the main culprit in periodontis, which results in devastation to the bone supporting the teeth. Adherence to oral surfaces is controlled through the tad (tight adherence) locus, which may express proteins that are involved in type IV secretion.
- Sequence; - BLASTN hit (Low score = Light, High score = Dark) - hypothetical protein; - cds: hover for description
General Information: This strain carries the anthrax toxin plasmid pXO1 but not the capsule plasmid pXO2 and is therefore avirulent but toxigenic. It is the counterpart to the Pasteur strain that carries pXO2 but not pXO1. This strain is often used for vaccine development. 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.