Buffaloes are more prone to parasitic diseases compared to Cattle¹. In India, fasciolosis in chiefly caused by Fasciola gigantica, having comparatively longer prepatent period and causing heavy morbidity and mortality. The present investigation records the incidence and pathological changes in the liver of buffaloes, naturally infected with Fasciola gigantica.

During the study a total number of 2119 livers were collected from buffaloes irrespective of sex, age groups and breeds from various abattoirs located in and around Bikaner and examined grossly. Out of these, representative pieces from 476 specimens showing gross lesions were collected in 10% buffered formol saline and processed to obtain paraffin embedded sections of 5 μ thickness which were stained by haematoxylin and eosin method for histopathological study⁵.

Out of 476 buffalo livers showing gross lesions, 68 (14.28%) had Fasciola infestation and exhibited varying degree of changes. The incidence of this condition in the present study was comparable to that reported by Kumar et al. (13.89%)⁴, but much lower to 86.5% reported earlier⁷. Grossly livers had numerous hemorrhagic areas under the capsule and extending variably into the parenchyma. Many of the bile ducts were prominent and thickened. The liver, was tougher than normal. Cut surface of liver showed the lodgment of the parasites in the bile ducts. The involved liver mostly appeared normal in size, however in some specimens liver surface was shrunken and rough showing increased fibrous tissue with bile ducts appearing dilated or protruding slightly above the cut surface of liver. These ducts contained numerous flukes admixed with a dirty gray or yellowish viscous, slimy fluid (Fig. 1). The large numbers of parasites were often encountered in the thickened bile ducts. Localized abscesses of various size were encountered mostly near the surface.

Macroscopically - In early stage parasites caused numerous haemorrhagic migratory tracts throughout the parenchyma with or without evidence of parasites. Advanced stage showed enlarged and thickened bile ducts, over all increased connective tissue and firm consistency of liver, and were in line to earlier observations³,⁶.

Microscopically, variety of lesions were found in the livers depending upon the stage and intensity of infestation. These were grouped as follows:-

Haemorrhagic lesions: These were considered as a consequence of early migration of immature fasciola in parenchyma. These lesions included accumulation of plasma and large number of erythrocytes (Fig. 2). Variable number of degenerated hepatocytes, congestion, reticulo-endothelial system response and infiltration of neutrophils, eosinophils and lymphocytes were usually seen in adjoining parenchyma. Further, in some instances peripheral part of lesions revealed fibroblasts and atrophied hepatocytes.

Necrotic lesions: These were minute necrotic foci found in liver infested with fluke. In necrotic area, disappearance of hepatocytes along with congested sinusoids and infiltration with macrophages, lymphocytes and a few polymorphs and eosinophils were often seen. The lesions were focal but not circumscribed and often accompanied with biliary ductular proliferation. In one case, the area showed changes typical of hemorrhagic necrosis.

Biliary and cirrhotic lesions: The bile ducts mostly appeared hyperplastic and degenerating with lymphocytic infiltration (Fig. 3). In one case, biliary ductular degeneration was prominent, where by most of the biliary ductules including the proliferated, showed eosinophilic contents⁹. Invagination of hyperplastic bile ducts and infiltration into surrounding parenchyma imparted adenoma like appearance. Fibrosis and lymphocytic infiltration often occurred simultaneously. At times, these infiltrations were very pronounced with resultant destruction and fibrosis. However, biliary ductual changes more often included biliary ductular proliferation and periductal fibrosis.

Frequently the portal tracts were enlarged and prominent having cellular infiltrations and fibrosis (Fig. 4) these extended variably in to the parenchyma at times joining the other portal tacts, so that the corresponding hepatic lobules were partly or completely surrounded by these extended and thickened fibrous tracts, often showing loss of central vein and columnar arrangement with atrophied or fatty hepatocytes in the corresponding lobules. Frequently the arterioles were sclerotic and some times central veins were also thickened.

Observation of haemorrhagic migratory tracks due to immature fluke migration in the form of considerable amount of plasma, large number of erythrocytes, disrupted hepatic columns, degenerated hepatocytes and inflammatory infiltrates corresponded with observations of Gresham and Jennings². Hyperplasic papillomatous and adenomatous bile ducts with or without lymphocytic infiltration, periductal fibrosis and accompanying atrophy of adjacent parenchyma were similar to those reported earlier³. Cirrhotic lesions particularly enlarged, prominent portal tracts with variable infiltration and fibrosis and their extension into parenchyma with or without pseudolobulation have also been reported³,⁸,⁹. Uncircumcised necrotic foci showing focal disappearance of hepatocytes with infiltration noted in the present tissues were comparable to earlier observations⁴.

Fig. 1:Cut surface of liver showing portal fibrosis (b), area of congesion (d) and Fasciola (a, c) parasite(s) in bile duct lumen.

Fig. 2:A. Photograph showing haemorrhagic track having accumulation of plasma and erythrocytes in the parenchyma with degeneration and necrosis. HE × 200.B. Grossly cut liver piece showing hydatid cyst wall (a) thickened bile duct having Fasciola (b).

Fig. 3:Photomicrograph showing Fasciola in the bile duct with mucosal hyperplasia and periductal fibrosis.

Fig. 4:Photomicrograph showing bile duct proliferation with periductal lymphocytic infiltration and fibrosis HE × 100.

Fasciola gigantica Induced liver pathology in buffaloes