In the recent years, modernisation of pig industry has been initiated to improve the husbandry practices for increased production as well as to prevent and control of important swine diseases. Despite these efforts, certain maladies like non-specific anorexia with poor body growth, frequent breakdown of immunity and subsequent mortality have been commonly encountered which shatters the economy of the poor and marginal farmers adopting pig farming. Aflatoxicosis is one of the most important factors largely responsible for these maladies. The geoclimatic condition of Assam is also congenial for the growth and propagation of the aflatoxin producing fungi. The present communication deals with one outbreak of aflatoxicosis in piglets of Base Pig Breeding Farm, Govt. of Assam while studying the aetiopathology of piglet mortality. Out of the total 125 piglets in the farm 11 piglets (8.8%) died due to aflatoxicosis.

The clinical signs included inappetence, dullness, depression and slight rise of temperature. The body coats were rough and a few piglets showed diarrhoea. Similar clinical signs were described by earlier workers²,⁸,⁹ in cases of aflatoxicosis in pigs. These signs might be due to metabolic disturbances produced by aflatoxin.

Grossly, the liver showed marked enlargement, mottling and pale yellowish discolouration with congestion. Irregular haemorrhagic areas were noticed on the visceral surface of the liver in addition to haemorrhagic gastroenteritis. Almost similar gross lesions were described in aflatoxicosis of pigs²,⁸,⁹. Congestion in kidneys, spleen and mesenteric lymph nodes as observed in the present cases closely resembled lesions described in earlier reports¹,⁹ which might be due to toxic injury to the vascular endothelium or anoxia².

Microscopically, the hepatic parenchyma showed congestion, haemorrhage and severe fatty changes (Fig. 1) involving whole lobules. Such lesions were also be described earlier¹,²,⁵. Aflatoxin markedly inhibits the biosynthesis of cholesterol and phospholipid as well as interferes with nucleic acid metabolism³,⁶. It could also a host response to mobilize fat from fat depot to the liver resulting in more accumulation of fats in the cytoplasm of hepatic cells. Fatty change might be a consequence of the failure of protein synthesis caused by aflatoxin⁴.

Fig. 1:Liver parenchyma showing severe fatty changes. HE × 400.

Fig. 2:Thickening of interlobular septa due to excessive infiltration of mononuclear cells. HE × 400.

Interlobular septa of hepatic parenchyma were thickened due to excessive infiltration of mononuclear cells (Fig. 2). This might be related to immunological response by the body. Periportal areas showed biliary epithelial cell proliferation. Many of the bile ducts were filled with proteinacious deposits. In other areas proliferating biliary epithelial cells showed tendency for new bile duct formation as described in previous reports⁷,². AFB₁ is excreted in the bile and finally through the faeces. Hence, it might be a response reflecting the attempt of the liver to get rid of the toxic material¹⁰. In the kidneys the renal parenchyma showed degenerative changes along with capillary congestion and mild diffuse haemorrhages with multiple cystic structures of variable sizes lined by a thin rim of connective tissue without any cellular reaction, indicating the lesion of hydronephrosis. This might be due to disturbances in protein synthesis. Quantitative analysis of feed sample revealed the level of aflatoxin at 254 ppb, which was slightly higher than the minimum level¹¹, sufficient to produce aflatoxicosis in piglets.

Aflatoxicosis in piglets: A pathological study