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.
- Sequence; - BLASTP hit: hover for score (Low score = Light, High score = Dark); - hypothetical protein; - cds: hover for description
General Information: This strain was isolated in the USA from the soft tick Ornithodoros turicatae. Borrelia turicatae is the causative agent of tick-borne relapsing fever in the southwestern USA. Ticks become infected with Borrelia while feeding on an infected mammal, usually a rodent or squirrel. Borrelia then multiplies rapidly, causing a generalized infection throughout the tick. While feeding, the tick passes the spirochete into a mammalian host through its infectious saliva. Relapsing fever is characterized by period of chills, fever, headache, and malaise, followed by an asymptomatic, followed by another episode of symptoms. The cycle of relapsing is due to changes in the surface proteins of Borrelia, which allow it to avoid detection and removal by the host immune system. This antigenic variation is the result of homologous recombination of silent proteins into an expressed locus, causing partial or complete replacement of one serotype with another. These plasmids carry genes involved in antigenic variation and pathogenicity.