Pre_GI: SWBIT SVG BLASTP

Query: NC_017062:33268 Rickettsia typhi str. B9991CWPP chromosome, complete genome

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

General Information: This genus, like other Rickettsial organisms such as Neorickettsia and Anaplasma, is composed of obligate intracellular pathogens. The latter is composed of two organisms, Rickettsia prowazekii and Rickettsia typhi. The bacteria are transmitted via an insect, usually a tick, to a host organism, in this case humans, 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. Transovarial transmission (from mother to offspring) occurs in the invertebrate host. This organism causes murine typhus and is an obligate intracellular pathogen that infects both the flea vector and hosts such as human, rat, and mouse. R. prowazekii, and genomic comparisons demonstrate colinearity and similarity to the genome of that organism except for two independent inversions near the origin and terminus. In the flea vector, the bacterium penetrates the gut epithelial barrier and is found in the feces which become infective.

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BLASTP 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.