Pre_GI: SWBIT SVG BLASTN

Query: NC_015571:2273503 Porphyromonas gingivalis TDC60, complete genome

Lineage: Porphyromonas gingivalis; Porphyromonas; Porphyromonadaceae; Bacteroidales; Bacteroidetes; Bacteria

General Information: This organism is associated with severe and chronic periodontal (tissues surrounding and supporting the tooth) diseases. Progression of the disease is caused by colonization by this organism in an anaerobic environment in host tissues and severe progression results in loss of the tissues supporting the tooth and eventually loss of the tooth itself. The black pigmentation characteristic of this bacterium comes from iron acquisition that does not use the typical siderophore system of other bacteria but accumulates hemin. Peptides appear to be the predominant carbon and energy source of this organism, perhaps in keeping with its ability to destroy host tissue. Oxygen tolerance systems play a part in establishment of the organism in the oral cavity, including a superoxide dismutase. Pathogenic factors include extracellular adhesins that mediate interactions with other bacteria as well as the extracellular matrix, and a host of degradative enzymes that are responsible for tissue degradation and spread of the organism including the gingipains, which are trypsin-like cysteine proteases.

Subject: NC_008011:663958 Lawsonia intracellularis PHE/MN1-00, complete genome

Lineage: Lawsonia intracellularis; Lawsonia; Desulfovibrionaceae; Desulfovibrionales; Proteobacteria; Bacteria

General Information: Lawsonia intracellularis PHE/MN1-00 was isolated from intestinal mucosal lesions in pigs that had proliferative enteropathy (PE). When introduced into health pigs, this organism produced the clinical and histological signs of PE. Causative agent for proliferative enteropathy in swine. This organism causes proliferative enteropathy (ileitis) in swine and other domesticated animals resulting in severe losses each year. This obligate intracellular pathogen infects the mucosa of the lower intestinal tract by initially infecting crypt cells, which are precursors that normally grow and divide in order to replace the epithelial cells. Once infection occurs, the crypt cells are stimulated to grow and divide abnormally, resulting in the proliferative phenotype. In severe cases of the disease the entire bowel can become affected and persist for up to 40 days, greatly affecting the host animal.