Abstract:
Canine babesiosis, which, in sub-Saharan Africa, is caused by the tick-transmitted intraerythrocytic
protozoan Babesia rossi, is one of the most common, clinically important tick-borne diseases of dogs
in the region. The disease in dogs occurs in two forms, namely uncomplicated and complicated
babesiosis. In the former, clinical signs are usually attributable to the effects of hemolysis. In
complicated canine babesiosis, the disease is attributable to the host’s immune response, with
overwhelming systemic inflammation and multiple organ dysfunction being associated with high
morbidity and mortality. The clinicopathological changes associated with complicated canine
babesiosis are similar to those reported in fatal malaria and sepsis in humans. There are not many
reports on the pathology of the liver in babesiosis and malaria. For the purpose of this study, liver
samples were collected from 10 dogs with fatal babesiosis. Haematology, serum biochemistry and
histologic data were compared with four healthy control dogs that were sourced from an animal
shelter. The most significant elevations in haematology values were decreases in red cell count,
haematocrit and platelet concentration, while the most significant increases in biochemistries were
increases in ALT and urea. The most significant histologic lesions in the Babesia-infected dogs included
dilation of the spaces of Disse due to oedema, cholestasis, hypertrophic Kupffer cells containing bile
and haemosiderin pigments, central venous and sinusoidal congestion, multifocal centrilobular
necrosis, inflammatory cell infiltrates consisting mostly of monocyte-macrophages (as determined by
MAC387, Iba-1 and CD204), and evidence of significant extramedullary haematopoiesis. The
hepatocytes showed numerous signs of cell injury such as presence of vesicular nuclei, hydropic
vacuolation and anisokaryosis. Most of these changes can be ascribed to severe haemolysis and the
associated hypoxia. Similar findings have been shown in the limited histomorphological studies on
babesiosis, human malaria, and in patients with sepsis. These results are also complimentary of
previous studies involving inflammatory cytokines and chemokines observed during the course of
babesiosis, with the most significant increases being IL-6, IL-10, MCP-1, and TNF-a, all of which are
monocyte-specific. These findings aid us in the understanding of the pathomechanisms behind the
disease and enable us better treat the symptoms that present.
