Liver histopathology in dogs with naturally acquired Babesia rossi infection

In sub-Saharan Africa, canine babesiosis, the most significant tick-borne disease in dogs, is primarily caused by the highly virulent intra-erythrocytic protozoan Babesia rossi, transmitted by ixodid ticks. The disease presents in two forms: uncomplicated and complicated. The former is characterized by hemolysis, while the latter involves severe systemic inflammation and multiple organ dysfunction, leading to high morbidity and mortality. Building on recent evidence of severe immunoinflammatory disruption in the spleen, lung, and bone marrow, this study examines liver histopathology in fatal Babesia rossi infection to determine whether the frequent hyperbilirubinemia and icterus of complicated babesiosis reflect primary hepatic injury or secondary systemic effects.

Liver samples from 10 dogs that succumbed to Babesia rossi infection were compared with samples from four healthy control dogs.

Significant hematological changes included reduced red cell count, hematocrit, and platelet concentration, while biochemical alterations showed increased serum ALT and urea. Key histopathological findings in the livers of Babesia-infected dogs showed severe diffuse dilation of the spaces of Disse, cholestasis, and hypertrophy of Kupffer cells containing bile and hemosiderin pigments. Additional findings included erythropoiesis, congestion, and widespread mononuclear inflammation, predominantly involving monocytes and macrophages with fewer lymphocytes and plasma cells, present in both intravascular and interstitial areas. Centrilobular hepatocytes exhibited coagulative necrosis or prominent hydropic vacuolation, likely attributable to severe hemolysis and resulting hypoxia, similar to findings reported in human malaria and sepsis.

These observations improve understanding of the pathomechanisms underlying fatal babesiosis in dogs, particularly its effects on the liver, and may help refine targeted treatment strategies.