Pre_GI: SWBIT SVG BLASTP

Query: NC_004603:3080614 Vibrio parahaemolyticus RIMD 2210633 chromosome I, complete

Lineage: Vibrio parahaemolyticus; Vibrio; Vibrionaceae; Vibrionales; Proteobacteria; Bacteria

General Information: This is a clinical strain isolated in 1996 in Osaka, Japan. It contains a type III secretion system which may enable colonization and penetration of the host intestinal epithelial layer, and possibly lead to septicemia. The genome contains multipe chromosomal rearrangements as compared to Vibrio cholerae. The organism also produces a hemolysin (thermostable direct hemolysin - TDH) that is particular to Vibrio parahaemolyticus. This genus is abundant in marine or freshwater environments such as estuaries, brackish ponds, or coastal areas; regions that provide an important reservoir for the organism in between outbreaks of the disease. Vibrio can affect shellfish, finfish, and other marine animals and a number of species are pathogenic for humans. This species causes food poisoning (gastroenteritis) in countries that have elevated levels of seafood consumption such as Japan.

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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.