Pre_GI: SWBIT SVG BLASTN

Query: NC_013515:550464 Streptobacillus moniliformis DSM 12112, complete genome

Lineage: Streptobacillus moniliformis; Streptobacillus; Leptotrichiaceae; Fusobacteriales; Fusobacteria; Bacteria

General Information: Isolation: Patient with rat-bite fever in France; Temp: Mesophile; Temp: 37C; Habitat: Host. Streptobacillus moniliformis causes rat bite fever, a systemic illness characterized by fever, chills, and joint pain which can progress to endocarditis, meningitis or pneumonia if left untreated. Although infection is usually associated with a rodent bite, this disease can be caused by ingestion of contaminated food or water. Streptobacillus moniliformis is the causative agent of rat bite fever in North and South America while a different organism, Spirillum minus, is primarily responsible for this disease in Asia and other countries.

- Sequence; - BLASTN hit (Low score = Light, High score = Dark)
- hypothetical protein; - cds: hover for description

BLASTN 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.