Intrahepatic vascular lesions in experimental and natural ovine fascioliasis.

Using acrylic resin casts prepared from the liver vasculature and histology, subdivisions of the portal and hepatic systems stenosed as a result of experimental and natural infections of F. hepatica were identified as terminal, secondary and tertiary portal veins and central and sublobular hepatic veins; primary portal veins were also involved in the experimentally infected livers. Fewer veins tended to be involved in livers naturally-infected and they were more evenly distributed among liver lobes than in the experimental disease where most were found in the ventral lobe. Casts of both types of infection also demonstrated enlargement and tortuosity of arteries in ventral lobes and those forming the peribiliary arterial plexus, as well as showing that multiple anastomotic channels had formed. The arterial changes and anastomoses were suggested as developing to compensate for the effects of vascular stenosis. Portal vein stenosis induced experimentally was the outcome of replacement of eosinophils and oedema-like fluid present in veins around fluke tracks and of the organisation of fluke tracts impinging upon veins. During the post-migratory period of infection, stenosis became more marked, for which no adequate cause was identified. In livers naturally-infected, in addition to stenosed portal and hepatic veins, vascular channels in collagen septa in sinusoids and a slight convolution of arteries were seen.