Pre_GI: SWBIT SVG BLASTN

Query: NC_010104:1096081 Brucella canis ATCC 23365 chromosome II, complete sequence

Lineage: Brucella canis; Brucella; Brucellaceae; Rhizobiales; Proteobacteria; Bacteria

General Information: Etiologic agent of canine brucellosis. They are highly infectious, and can be spread through contact with infected animal products or through the air, making them a potential bioterrorism agent. Once the organism has entered the body, it can become intracellular, and enter the blood and lymphatic regions, multiplying inside phagocytes before eventually causing bacteremia (spread of bacteria through the blood). Virulence may depend on a type IV secretion system which may promote intracellular growth by secreting important effector molecules. This bacterium is the causative agent of canine brucellosis. The main sources of infection are vaginal fluids of infected females and urine in males. The most significant symptoms are late abortions in bitches, epididymitis in males and infertility in both sexes, as well as generalized lymphadenitis, discospondylitis and uveitis. Human contagion is not frequent, although it has been reported, and is easily treated. B. canis can be differentiated from the other species of the genus Brucella (except B. ovis) in that it forms rugose colonies.

Subject: NC_005956:1402500 Bartonella henselae str. Houston-1, complete genome

Lineage: Bartonella henselae; Bartonella; Bartonellaceae; Rhizobiales; Proteobacteria; Bacteria

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.