Query: NC_008710:621822 Borrelia turicatae 91E135, complete genome Lineage: Borrelia turicatae; Borrelia; Spirochaetaceae; Spirochaetales; Spirochaetes; Bacteria 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.
- Sequence; - BLASTP hit: hover for score (Low score = Light, High score = Dark); - hypothetical protein; - cds: hover for description
General Information: Bartonella henselae str. Houston-1 (ATCC 49882) was isolated from human blood in Houston Texas. Causative agent of cat scratch fever. This group of alpha proteobacteria are unique among pathogens in that they cause angiogenic lesions. This organism was identified as the causative agent of cat scratch fever, a disease found commonly in children or in immunocompromised adults. 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.