Pre_GI: SWBIT SVG BLASTN

Query: NC_011094:1127983 Salmonella enterica subsp. enterica serovar Schwarzengrund str

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

General Information: This serovar is the predominant cause of Salmonellosis in Southeast Asia, a major source of imported food products to the USA. It was also the cause of the first recognized outbreak of fluoroquinolone-resistant salmonellosis in the USA. Recent reports suggest that high-level fluoroquinolone resistance is emerging in S. Schwarzengrund in different parts of the world. 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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BLASTN Alignment.txt

Subject: NC_005956:1019788 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.