Pre_GI: SWBIT SVG BLASTN

Query: NC_008369:1702885 Francisella tularensis subsp. holarctica OSU18, complete genome

Lineage: Francisella tularensis; Francisella; Francisellaceae; Thiotrichales; Proteobacteria; Bacteria

General Information: Isolated from a beaver that died of tularemia in Oklahoma in 1978. Causative agent of tularemia. This organism was first identified by Edward Francis as the causative agent of a plague-like illness that affected squirrels in Tulare county in California in the early part of the 20th century. The organism now bears his name. The disease, which has been noted throughout recorded history, can be transmitted to humans by infected ticks or deerflies, infected meat, or by aerosol, and thus is a potential bioterrorism agent. This organism has a high infectivity rate, and can invade phagocytic and nonphagocytic cells, multiplying rapidly. Once within a macrophage, the organism can escape the phagosome and live in the cytosol. It is an aquatic organism, and can be found living inside protozoans, similar to what is observed with Legionella.

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BLASTN Alignment.txt

Subject: NC_005956:1572500 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.