Pre_GI: SWBIT SVG BLASTP

Query: NC_009879:860925 Rickettsia canadensis str. McKiel, complete genome

Lineage: Rickettsia canadensis; Rickettsia; Rickettsiaceae; Rickettsiales; Proteobacteria; Bacteria

General Information: This organism was originally isolated from ticks in a field study on tick-transmitted diseases of small mammals in Canada. Member of the typhus group of Rickettsiales. Members of this genus, like other Rickettsial organisms such as Neorickettsia and Anaplasma, are obligate intracellular pathogens. In both groups, the bacteria are transmitted via an insect, usually a tick, to a host organism where they target endothelial cells and sometimes macrophages. They attach via an adhesin, rickettsial outer membrane protein A, and are internalized where they persist as cytoplasmically free organisms. Rickettsia canadensis was originally thought to be a member of the typhus group of Rickettsiales, however, it is now thought to represent a distict group with the rickettsia.

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BLASTP Alignment.txt

Subject: NC_005956:699206 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.