Neoplasms of the duck with special reference to hepatocarcinogenesis
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Date
1992
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Centre of Excellence in Pathology, College of Veterinary and Animal Sciences, Mannuthy
Abstract
At the Centre of Excellence in Pathology during the period from 1989 – 1991 six hundred and eighteen ducks were subjected to detailed post – mortem examination and out of this one hundred and thirty six ducks showed hepatosis, one hundred and twenty six ducks had hepatitis and sixteen ducks had hepatic tumours.
At the Government duck farm, Niranam, 14,360 ducks were examined and 46.92 per cent of ducks had hepatic lesions. However, tumours were not recorded. The possible aetiological role of aflatoxin for hepatosis and hepatic tumour was indicated.
An experiment was designed taking duck as a model to assess the carcinogenic affect of genotoxic carcinogen aflatoxin and non – genotoxic carcinogen clofibrate. Aflatoxin was administered to twelve ducks at the dose rate of 0.04165 mg/kg body weight every third day for a period of six months. Hepatic tumours were recorded in four ducks out of the six ducks sacrificed on the 90th day and in all the six ducks sacrificed on the 180th day.
The body weight, haemoglobin, ESR, total serum protein, albumin, globulin, serum enzymes such as AST, ALT, GGT and ALP were estimated at fortnightly intervals.
Clinically there was reduction in the body weight, haemoglobin, total serum protein, albumin and globumin levels by the third month. There was significant increase in ESR, serum AST, ALT, GGT and ALP levels when compared to the control ducks. These clinical changes were attributed to hepatosis and heapatic tumours.
Hepatosis characterised by moderate to severe enlargement of the liver with scattered greyish white nodules of varying sizes were the chief lesions encountered in aflatoxin fed ducks at autopsy.
The tumours encountered were classified as hepatocellular carcinoma (6) and cholangiocellular carcinoma (4). The gross and histopathological features of these lesions were described in detail. Histochemically the activity of GGT and ALP was moderate to severe in the liver tumours. The sequence of histological changes seen was hapatic degeneration necrosis and tumour formation.
Clofibrate was given at the dose rate of 0.05 g/kg body weight per day for six months. In these ducks the liver has a cooked appearance with few focal greyish white patches when sacrificed at the sixth month.
There was significant reduction in the body weight, haemoglobin, total serum protein, albumin and globulin levels and serum cholesterol level at the third and sixth month. However, ESR, serum SGOT, SGPT, GGT and ALP showed significant increase as compared to the control ducks. These clinical parameters suggested hepatosis.
Histologically there was moderate fatty change, focal disassociation of hepatocytes and biliary hyperplasia. Histochemical expression of ALP was moderate to intense in the liver and there was moderate to severe proliferation of peroxisomes. There was histological evidence of preneoplastic changes although no tumours were seen.
By this investigation the high sensitivity of ducks to aflatoxin was clarified and the tumour induction potential of afiatoxin in ducks was evaluated and the nature of hepatic tumours induced and delineated.
Clofibrate was demonstrated to induce hepatosis and preneoplastic changes in the hepatic tissue and the possible carcinogenic potential of clofibrate was indicated.
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Citation
170363