Query: NC_010161:1844452 Bartonella tribocorum CIP 105476, complete genome Lineage: Bartonella tribocorum; Bartonella; Bartonellaceae; Rhizobiales; Proteobacteria; Bacteria General Information: This organism was isolated from the blood of wild rats and from fleas obtained from wild rats. Transmission of these organisms is often through an insect vector. Once in a host, this intracellular pathogen is internalized by an actin-dependent mechanism, and primarily targets endothelial cells, although other cells can be infected. The proliferation of the vascular endothelium (bacillary angiomatosis) is characterisitic of Bartonella infection and results in multiplication of the bacterium's host cells. Infected macrophages are stimulated to release vascular endothelial growth factor (VEGF) and interleukin 1 beta, both of which promote angiogenesis. Endothelial cells are also stimulated to grow and divide by direct contact with bacterial cells. In addition, programmed cell death (apoptosis) of endothelial cells is inhibited, combatting a common mechanism eukaryotic cells use to deal with bacterial infection. Other pathogenicity factors include pili and outer membrane adhesins for attachment to host cells. This organism is genetically related to Bartonella elizabethae which was isolated from a case of endocarditis in a human.
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General Information: This strain (also known as HG66) is virulent in a mouse model and has been extensively studied. It was originally isolated by H. Werner in the 1950s in Bonn, Germany, from an unknown human infection. Associated with severe and chronic periodontal disease. 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.