Abstract
BackgroundThis paper describes liver cirrhosis in 35 fallow deer infected with the giant liver fluke, as well as the distribution, origin, and role of myofibroblasts in its development.ResultsIn liver of infected deer, stripes of connective tissue are wound around groups of degenerated and regenerated liver lobuli. In the connective tissue, lymphocytes and macrophages which often contain parasite hematin are also present. The walls of the bile ducts are thickened, the epithelium multiplied with mucous metaplasia, and desquamated cells, parasite eggs and brown pigment are present in their lumen.In the livers with cirrhosis, immunopositivity to α-SMA and desmin was observed in cells in portal and septal spaces, at the edge between fibrotic septa and the surrounding parenchyma and in perisinusoidal spaces. These cells vary in size, they are round, oval, spindle-shaped or irregular in shape, similar to vascular smooth muscle cells. The derangement of epithelial-mesenchymal interactions detected in chronic cholangiopathies is most probably the pro-fibrogenic mechanism in liver cirrhosis of fallow deer (Dama dama) infected with the giant liver fluke (Fascioloides magna).ConclusionMyofibroblasts, especially hepatic stellate cells (HSCs), play an important role in the synthesis of extracellular matrix components in the development of parasitic fibrosis and cirrhosis in the liver of fallow deer.
Highlights
This paper describes liver cirrhosis in 35 fallow deer infected with the giant liver fluke, as well as the distribution, origin, and role of myofibroblasts in its development
The finding of this parasite in the fallow deer population represents a threat as the giant liver fluke could spread to domestic ruminants which reside in close proximity to hunting grounds [1,4,5,7,8,9]
This paper is focused on pathohistological changes in the liver of fallow deer with parasitic cirrhosis caused by the giant liver fluke and the heterogeneity of the hepatic myofibroblast population
Summary
This paper describes liver cirrhosis in 35 fallow deer infected with the giant liver fluke, as well as the distribution, origin, and role of myofibroblasts in its development. The giant liver fluke originates from North America, from where it spread to other regions through imports of deer game. The bile duct walls are thickened, and desquamated cells, parasite eggs and brown pigment are present in their lumen [1,6,7,8,9]. These changes are somewhat similar to those described in the liver of domestic ruminants in connection with infection with the big liver fluke Fasciola hepatica. Liver fibrosis and cirrhosis develop as the ultimate result of chronic liver damage caused by F. hepatica [10,11,12,13]
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