Query: NC_002488:2502000 Xylella fastidiosa 9a5c, complete genome
Lineage: Xylella fastidiosa; Xylella; Xanthomonadaceae; Xanthomonadales; Proteobacteria; Bacteria
General Information: This strain was derived from a pathogenic strain (8.1b) isolated in 1992 in France that had come from infected twigs derived from the sweet orange strain Valencia in Brazil in the same year. This organism was first identified in 1993 as the causal agent of citrus variegated chlorosis, a disease that affects varieties of sweet oranges. Other strains of this species cause a range of diseases in mulberry, pear, almond, elm, sycamore, oak, maple, pecan and coffee which collectively result in multimillion dollar devastation of economically important plants. Xylella fastidiosa is similar to Xanthomonas campestris pv. campestris in that it produces a wide variety of pathogenic factors for colonization in a host-specific manner including a large number of fimbrial and afimbrial adhesins for attachment. It does not contain a type III secretion system, but possesses genes for a type II secretion system for export of exoenzymes that degrade the plant cell wall and allow the bacterium to colonize the plant xylem.
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.