Toxicopathological studies on the effects of T-2 mycotoxin and their interaction in juvenile goats

Abstract

Food and feeds contaminated with mycotoxins have been a threat to the rearing industry by causing some of the most fatal toxic reactions not only in the farm animals but also in humans who consume them. Toxicity to juvenile goats was induced by feed contamination with T-2 toxin (at 10 and 20 ppm dosage; group I and II, respectively). The toxicity impact was assessed on days 15 and 30 post treatment with respect to growth performance, oxidative stress, apoptotic studies and detailed pathomorphology. The study revealed that apart from the obvious clinical toxicosis (weakness, lethargy, and retardation in growth), the toxin fed groups also exhibited significant haematological (reduced hemoglobin, total leukocyte and thrombocyte counts) and biochemical changes (increased levels of oxidative stress markers with concomitant decrease in levels of serum and tissue catalase and superoxide dismutase). The pathomorphological and histological alterations suggested that the liver and intestine were the most affected organs. Ultra-structurally, varying degrees of degeneration, cytoplasmic vacuolations and pleomorphic mitochondria were observed in the hepatocytes and the enterocytes of the intestine. Kidney also revealed extensive degeneration of the cytoplasmic organelles with similar condensation of the heterochromatin whereas the neuronal degeneration was characterized by circular, whirling structures. In addition, the central vein and portal triad of the hepatocytes, cryptic epithelial cells of the intestine, MLNs in the lymphoid follicles, PCT and DCT of the nephronal tissues and the white pulp of the spleen exhibited extensive apoptosis. In this study, it was also observed that the expression of HSPs, pro-apoptotic proteins and pro-inflammatory cytokines were significantly upregulated in response to the toxin treatment. These results suggest that the pathogenesis of T-2 toxicosis in goats employs oxidative, apoptotic and inflammatory mechanisms.

Fig 1. Liver (group 1, 15 days): epithelial hyperplasia with bile ducts having degeneration of hepatocytes.

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Fig 2. Liver (group 1, 30 days): individual cell necrosis with dark pyknotic nucleus in the parenchyma with diffuses fatty changes of hepatocytes.

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Fig 3. Liver (group 2, 15 days): Hypertrophy peri-billiary hyperplasia/fibrosis with bile ducts having cell debris and diffuse centrilobular necrosis of hepatocytes.

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Fig 4. Liver (group 2, 30 days): Hepatocytes showing distinct dark nucleus and homogeneous deep eosinophilic cytoplasm called as ‘Ghost hepatocytes’.

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Fig 5. Intestines (group 1, 15 days): Lamina propria showing diffusely infiltrated with necrotic lymphocytes, nuclear pyknosis and fragmentation.

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Fig 6. Intestines (group 2, 15 days): Lamina propria showing depletion/lymphocytolysis in Peyer’s patches.

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Fig 7. Intestines (group 2, 30 days): Crypts in lamina propria showing diffuse epithelial necrosis with fragmentation of nuclei, disruption of BM and necrosis of lymphocytes.

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Fig 8. Mesenteric lymph nodes (group 1, 30 days): Widespread depletion in cortical follicles with diffuse necrosis of lymphocytes/lymphocytolysis.

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Fig 9. Mesenteric lymph nodes (group 2, 30 days): Lymphoid depletion and infiltration of large polygonal epithelioid cells and macrophages.

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Fig 10. Kidney (group 1, 30 days): Epithelial cells of DCT showing detachment, degeneration of vacuoles and occurrence of granular pink matter in the lumen.

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Fig 11. Kidney (group 2, 30 days): Degeneration of PCT and DCT showing loss of nuclei and brush borders.

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Fig 12. Spleen (group 1, 30 days): Follicles showing depletion and necrosis of lymphocytes around the central artery.

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Fig 13. Spleen (group 2, 30 days): Epithelioid cells reactions in the white pulp leading to lymphocytolysis.

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Fig 14. Brain (group 2, 30 days): Neurons showing shrinkage and degeneration with eosinophilic cytoplasm indicating satellitosis.

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Fig 15. Liver (group 2, 30 days): Mitochondrial degeneration with loss of cristae and formation of empty spaces in the cytoplasm of hepatocytes.

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Fig 16. Liver (group 2, 30 days): Hyperplasticity in the collagen fibers of liver.

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Fig 17. Small intestine (group 2, 30 days): Heterochromatin showing condensation, margination and clumping with indistinct nuclear membrane in enterocytes.

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Fig 18. Kidney (group 2, 30 days): Epithelial cells showing loss of cristae leading to mitochondria pleomorphic.

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Fig 19. Brain (group 2, 30 days): Degeneration of neurons by formation of circular, whirling dark structures called as myelin figures.

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Fig 20. Liver (group 1, 30 days): Apoptosis in hepatocytes around central vein and portal triad.

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Fig 21. Small intestine (group 1, 30 days): Apoptosis in cryptic epithelial cells of the small intestine.

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Fig 22. Small intestine (group 2, 30 days): Peyer’s patches in intestine showing apoptotic lymphocytes.

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Fig 23. Mesenteric lymph nodes (group 2, 30 days): Apoptotic lymphocytes in the follicles of MLN.

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Fig 24. Kidney (group 2, 30 days): PCT and DCT showing apoptotic epithelial cells.

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Fig 25. Spleen (group 2, 30 days): Apoptotic lymphocytes in white pulp area of spleen.

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