Bartonella and Afipia

Published on 08/02/2015 by admin

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Last modified 08/02/2015

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Bartonella and Afipia

The two genera, Bartonella and Afipia, are able to grow on chocolate agar and, albeit very slowly, on routine blood (trypticase soy agar with 5% sheep blood agar), typically appearing after 12 to 14 days and sometimes requiring as long as 45 days; neither organism grows on MacConkey agar. Presently, there is no optimal procedure for the isolation of these organisms from clinical specimens. Because of these similarities and because two organisms, Bartonella henselae and Afipia felis, cause cat-scratch disease (CSD), these genera are addressed together in this chapter.

Bartonella

General Characteristics

Bartonella spp. were previously grouped with members of the family Rickettsiales. However, because of extensive differences, the family Bartonellaceae was removed from this order. As a result of phylogenetic studies using molecular biologic techniques, the genus Bartonella currently includes 22 species and subspecies, most of which were reclassified from the genus Rochalimeae and from the genus Grahamella. Only five species are currently recognized as major causes of disease in humans (Table 33-1), but other members of the genus have been found in animal reservoirs such as rodents, ruminants, and moles. Bartonella spp. are most closely related to Brucella abortus and Agrobacterium tumefaciens and are short, gram-negative, rod-shaped, facultative intracellular, fastidious organisms that are oxidase negative and grow best on blood-enriched media or cell co-culture systems.

TABLE 33-1

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

Organism Habitat (Reservoir) Mode of Transmission Clinical Manifestation(s)
Bartonella alsatica Rabbits Unknown; fleas or ticks suspected Humans accidental hosts
B. bacilliformis Uncertain; humans; possibly cats and dogs Fleas and sandflies Carrión’s disease*
B. quintana Uncertain; small rodents, gerbils, humans Human body louse and fleas
B. henselae Domestic cats Domestic cats and dogs; bites or scratches, fleas
B. clarridgeiae Domestic cats Domestic cat; bites or scratches and fleas
B. elizabethae Rats Fleas Endocarditis

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Note: Other Bartonella species have caused incidental infections in humans, but only one or a few cases have been documented.

*Disease confined to a small endemic area in South America; characterized by a septicemic phase with anemia, malaise, fever, and enlarged lymph nodes in the liver and spleen, followed by a cutaneous phase with bright red cutaneous nodules, usually self-limited.

Epidemiology and Pathogenesis

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 Table 33-1.

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.