General Information: This organism was isolated from the blood of wild rats and from fleas obtained from wild rats. Transmission of these organisms is often through an insect vector. Once in a host, this intracellular pathogen is internalized by an actin-dependent mechanism, and primarily targets endothelial cells, although other cells can be infected. 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. This organism is genetically related to Bartonella elizabethae which was isolated from a case of endocarditis in a human.