Pre_GI: SWBIT SVG BLASTP

Query: NC_007633:952728 Mycoplasma capricolum subsp. capricolum ATCC 27343, complete

Lineage: Mycoplasma capricolum; Mycoplasma; Mycoplasmataceae; Mycoplasmatales; Tenericutes; Bacteria

General Information: Pathogen of goats. This genus currently comprises more than 120 obligate parasitic species found in a wide spectrum of hosts, including humans, animals, insects and plants. The primary habitats of human and animal mycoplasmas are mucous membranes of the respiratory and urogenital tracts, eyes, mammary glands and the joints. Infection that proceeds through attachment of the bacteria to the host cell via specialized surface proteins, adhesins, and subsequent invasion, results in prolonged intracellular persistence that may cause lethality. Once detected in association with their eukaryotic host tissue, most mycoplasmas can be cultivated in the absence of a host if their extremely fastidious growth requirements are met.

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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.