Organisms belonging to the genus Bartonella cause numerous infections in humans; most of these infections are thought to be zoonoses. Interest in these organisms has increased because of their recognition as causes of an expanding array of clinical syndromes in immunocompromised and immunocompetent patients. For example, Bartonella species have been recognized with increasing frequency since the early 2000s as a cause of culture-negative endocarditis. Humans acquire infection either naturally (infections caused by Bartonella quintana or Bartonella bacilliformis) or incidentally (other Bartonella species) via arthropod-borne transmission. Nevertheless, questions remain regarding the epidemiology of these infections; some epidemiologic information is summarized in Table1.

Table1. Organisms Belonging to the Genus Bartonella and Recognized to Cause Disease in Humans*

Bartonella is a facultative intracellular bacterium that closely interacts with the host cells and has unique abilities to cause either acute or chronic infection as well as the proliferation of microvascular endothelial cells and angiogenesis (forming new capillaries from preexisting ones) or suppurative manifestations. Three Bartonella species (B. quintana, B. bacilliformis, and B. henselae) are capable of causing angiogenic lesions. Research has demonstrated that some species are capable of interacting with host red blood cells, endothelial cells, and possibly bone marrow progenitor cells. Colonization of vascular endothelium is considered a crucial step in the establishment and maintenance of Bartonella-triggered angioproliferative  lesions. Within several hours following infection of cultured human umbilical vein endothelial cells, Bartonella species adhere to and enter these cells by an actin-dependent process resembling other bacterial directed phagocytosis or uptake into host cells. Recent studies have also shown that B. henselae possess nine outer membrane proteins (OMP), one of which is able to bind to endothelial cells.

Typically, Bartonella species multiply and persist in the red blood cells in the reservoir host and share common persistence and dissemination strategies. In addition to angioproliferation, recent data indicate bartonellae can inhibit endothelial cell apoptosis (programmed cell death); these organisms also activate monocyte and macrophage cells capable of producing potent angiogenic factors. Although more research is needed regarding the pathogenesis of infections caused by Bartonella, it is evident these organisms possess unique pathogenic strategies to expand their bacterial niche in order to sustain survival within the human host. It is evident that the pathologic response to these infections varies substantially with the status of the host immune system. For example, infection with the same Bartonella species, such as B. henselae, can cause a focal suppurative reaction (i.e., CSD) in immunocompetent patients or a multifocal angioproliferative lesion (i.e., bacillary angiomatosis) in immunocompromised patients. B. quintana, the etiologic agent for trench fever, also causes bacillary angiomatosis in immunocompromised patients.

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