Pre_GI: SWBIT SVG BLASTP

Query: NC_006511:3364448 Salmonella enterica subsp. enterica serovar Paratyphi A str. ATCC

Lineage: Salmonella enterica; Salmonella; Enterobacteriaceae; Enterobacteriales; Proteobacteria; Bacteria

General Information: This serovar has a narrow host range and causes a typhoid-like (paratyphoid fever) illness in humans. It is especially prevalent in southern and eastern Asia, and has been associated with some particularly virulent outbreaks. A number of isolates are increasingly antibiotic resistant. Causes enteric infections. This group of Enterobactericiae have pathogenic characteristics and are one of the most common causes of enteric infections (food poisoning) worldwide. They were named after the scientist Dr. Daniel Salmon who isolated the first organism, Salmonella choleraesuis, from the intestine of a pig. The presence of several pathogenicity islands (PAIs) that encode various virulence factors allows Salmonella spp. to colonize and infect host organisms. There are two important PAIs, Salmonella pathogenicity island 1 and 2 (SPI-1 and SPI-2) that encode two different type III secretion systems for the delivery of effector molecules into the host cell that result in internalization of the bacteria which then leads to systemic spread.

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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.