Mechanisms Involved in the Persistence of Babesia canis Infection in Dogs

Abstract

Dogs that are infected with Babesia canis parasites usually show severe clinical signs, yet often very few parasites are detectable in the blood circulation. The results showed that large numbers of B. canis-infected red blood cells accumulate in the microvasculature of infected subjects. The initial process leading to the attachment of infected erythrocytes to the endothelial cells of small capillaries (sequestration) appears to involve the interaction of parasite molecules at the erythrocyte surface with ligands on the endothelial cells. Since parasites continue to develop in the sequestered erythrocyte, it would be expected that the infected erythrocyte is destroyed when the mature parasites escape the host cell, which would make it hard to explain accumulation of infected erythrocytes at the initial site of attachment. Apparently, additional processes are triggered that lead to consolidation of parasite sequestration. One possible explanation is that after initial attachment of an infected erythrocyte to the wall of a blood capillary, the coagulation system is involved in the trapping of infected and uninfected erythrocytes. The data further suggest that newly formed parasites subsequently infect normal red blood cells that are also trapped in the capillary, which finally leads to capillaries that appear to be loaded with infected erythrocytes.

Detection of Anaplasma phagocytophilum, Babesia odocoilei, Babesia sp., Borrelia burgdorferi Sensu Lato, and Hepatozoon canis in Ixodes scapularis Ticks Collected in Eastern Canada

“…When B. odocoilei-infected red blood cells adhere to fibrin, which line the endothelial cells of capillaries and venules, cytoadherence (binding to endothelial cells) and sequestration result. This fibrin-bonding mechanism is similar to the sequestration discerned with B. canis in dogs [42]. Cytoadherence and sequestration develop as the microvasculature of capillaries and venules fill up with infected erythrocytes.…”

Applying Machine Learning to Predict the Exportome of Bovine and Canine Babesia Species That Cause Babesiosis

“…Taken together, these two biological facts reinforce current understanding that it is entirely proteins exported from the parasite and not from the host cell that alter structural and functional properties of parasitised RBCs (pRBCs) [10,15]. One alteration is the insertion of parasite molecules at the pRBC surface [16]. These molecules appear to be involved in the attachment of pRBCs to ligands on endothelial cells of blood vessels, a process called sequestration [16,17].…”

“…In contrast, the ridge-like structures are completely absent on the surface of B. bigemina [5] and B. canis pRBCs [16]. Both of these species, however, still express parasite antigens at the pRBC surface and cause acute and persistent babesiosis [16,20], although B. bigemina has a relatively reduced virulence compared to B. bovis [20]. All proteins exported from Babesia into the host RBC cytoplasm and/or the RBC membrane (collectively called the exportome) are highly worthy of further investigation.…”

“…One alteration is the insertion of parasite molecules at the pRBC surface [16]. These molecules appear to be involved in the attachment of pRBCs to ligands on endothelial cells of blood vessels, a process called sequestration [16,17]. Sequestration is an important contributor to the sequence of events that leads to babesiosis.…”

“…This increased rigidity reduces the overall pRBC deformability, which has been shown to contribute to babesiosis development [19]. In contrast, the ridge-like structures are completely absent on the surface of B. bigemina [5] and B. canis pRBCs [16]. Both of these species, however, still express parasite antigens at the pRBC surface and cause acute and persistent babesiosis [16,20], although B. bigemina has a relatively reduced virulence compared to B. bovis [20].…”