Pathogenesis and Transmission
Fleas play a major role in the transmission of Bartonella, particularly in felines (B. henselae). Due to their ubiquitous nature and spread through animal transport, fleas pose a worldwide risk for cats and dogs to become infected with Bartonella spp. But also other potential vectors for Bartonella transmission, such as ticks and biting flies, have been identified.
Due to the fact that dogs which are seropositive to B. vinsonii subsp. berkhoffii are often seropositive to Ehrlichia canis and/or Babesia canis at the same time, the transmitting tick vector, Rhipicephalus sanguineus, has been suggested as a likely vector also for Bartonella spp.
Different arthropod vectors have been reported for different Bartonella spp. Confirmed vectors are the cat flea (Ctenocephalides felis) for B. henselae, B. clarridgeiae, B. koehlerae, the sand fly (Lutzomyia verrucarum) for B. bacilliformis, the human louse (Pediculus humanus humanus respectively Pediculus humanus corporis) for B. quintana and the rat flea (Xenopsylla cheopis) for B. elizabethae.
Further suspected vectors for Bartonella comprise different species of fleas, sandflies, mites, biting flies and flies.
Besides transmission via blood-feeding arthropods, mechanical transmission of Bartonella spp. by biting and scratching also poses a risk for human infection as well known for the cat scratch disease.
Bartonella spp. infect erythrocytes, endothelial cells and macrophages, often leading to persistent blood-borne infections. Location within erythrocytes and also within vascular endothelial cells is believed to protect Bartonellae from antimicrobial agents. Immune system avoidance via intracellular location, frequent genetic rearrangements, and alteration of outer membrane proteins, is also considered important.
In dogs, B. vinsonii subsp. berkhoffii causes chronic infections by establishing intracellular infection in erythrocytes and endothelial cells, thereby escaping the acquired humoral and cell-mediated immune defenses of the host. Infection with B. vinsonii subsp. berkhoffii might induce a degree of chronic immunosuppression that could predispose dogs to infections with other pathogenic agents, resulting in a wide array of clinical manifestations in naturally-infected dogs.
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