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Immunopathological studies in experimental T-2 toxicosis in wistar rats

By: Ghafoor, S. R. A.
Material type: materialTypeLabelBookPublisher: Izatnagar IVRI 2011Description: 148p.Subject(s): VETERINARY PATHOLOGYDDC classification: 636.089607 G341I Dissertation note: Thesis (Ph D) Deemed University,IVRI 2011 Sharma, A. K. Summary: The present study was designed to investigate immunopathology and pathomorphology in T- 2 toxicosis in rats and to make comparative evaluation of conventional methods vis-a-vis-ELISA for detection of T-2 toxin in feed. Four groups of male Wistar rats (48 rats of 4 weeks age each) received T-2 toxin in feed respectively at 0.5, 0.75, 1.0 ppm and 0.0 levels for 12 weeks. Eight rats each were sacrificed at 2, 4, 6, 8, 10 and 12 weeks intervals. The clinical signs exhibited were variable degree of dullness, weakness, lethargy, retardation in growth, rough hair coat, disinclination to move and reduced feed intake, the severity of which was dose and duration dependent. In 1.0 ppm dose group gangrenous dermatitis of tail and facial and podal dermatitis with mortality of 12.0% were also noticed. Significant haematobiochemical observations included anaemia, leucopaenia, lymphocytopaenia, thrombocytopenia, hypoproteinemia with decreased albumin: globulin ratios, hypoglycaemia and increased serum ALT, AST and LDH activities, and increase in BUN and serum creatinine levels. Significant reduction in IgG, IgM, IgA levels, HA titres against SRBCs, DTH with ovalbumin, amount of NO production by resident peritoneal macrophages, SI indices, number of CD4+ and CD8+ and CD4+: CD8+ ratios in peripheral blood and down regulation of different cytokines like IFN- ?, IL-2 and IL-4 and upregulation of IL-10 were recorded in T-2 treated rats suggested suppression of AMI and CMI due to T-2 toxicity. Significant increase in the MDA levels with decrease in SOD, catalase and GSH levels in kidneys, liver, brain, testes and spleen indicated cell injury in T-2 toxicity due to free radical induced oxidative stress. Grossly, kidneys and livers were pale and enlarged and spleen, thymus and testes were atrophic in T-2 treated animals. Histopathologically, most consistent lesions included swollen and vacuolated epithelial cells of PCTs with occasional necrosis and presence of proteinaceous and cellular casts in the lumen, congestion of intertubular blood vessels, mononuclear cells infiltration in interstitium, swollen parietal epithelial cells of Bowman’s capsule and dilatation of DCTs in kidneys; swollen hepatocytes with granular or vacuolated cytoplasm, karyomegaly, double nuclei with anisokaryosis, proliferation of bile ductules and mononuclear cell infiltration in the portal areas in liver; engorged blood vessels, haemorrhages, degeneration and thining of muscle fibres with increased inter fascicular spaces in heart; engorgement of blood vessels with increased perivascular spaces, occasional perivascular cuffing, increased perineuronal spaces and focal haemorrhages and gliosis in cerebrum, severe degeneration and depletion of Purkinje cells in cerebellum; lymphoid cells depletion and presence of large number of multinucleated megakaryocytes in spleen; lymphoid cells depletion, lymphocytolysis, congestion and hemorrhage in interfollicular spaces, extensive proliferation of interfollicular connective tissue causing atrophy in thymus; lymphoid cells depletion in Peyer’s patches; degeneration and disorganization of spermatogonial cells with reduced spermatogenesis in testes; reduced number of spermatozoa in epididymal ductules and extensive vacuolation and necrosis of cortical cells with presence of interstitial MNCs infiltration in adrenal cortices. Fifty feed samples were analysed for T-2 toxin by TLC and spectrophotometry and by competitive ELISA. Thirteen samples were found positive by ELISA only with T-2 levels 0.120 ppm to 0.235 ppm. Five T-2 negative samples were spiked with known amount (0.05-10μg/g) of T-2 toxin. The lowest detection limit was found to be 0.5 μg/g for TLC and Spectrophotometry and 0.125 μg/g for ELISA. It was concluded that T-2 toxin produced significant toxicopathological changes in a dose and duration dependent manner. It was found to be nephrotoxic, hepatotoxic and immunosuppressive. The tissue damage was due to free radical induced oxidative stress. ELISA was found to be more sensitive method for detecting T-2 toxin in feed than TLC and spectrophotometry.
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Thesis (Ph D) Deemed University,IVRI 2011 Sharma, A. K.

The present study was designed to investigate immunopathology and pathomorphology in T-
2 toxicosis in rats and to make comparative evaluation of conventional methods vis-a-vis-ELISA for
detection of T-2 toxin in feed. Four groups of male Wistar rats (48 rats of 4 weeks age each) received T-2
toxin in feed respectively at 0.5, 0.75, 1.0 ppm and 0.0 levels for 12 weeks. Eight rats each were sacrificed
at 2, 4, 6, 8, 10 and 12 weeks intervals. The clinical signs exhibited were variable degree of dullness,
weakness, lethargy, retardation in growth, rough hair coat, disinclination to move and reduced feed
intake, the severity of which was dose and duration dependent. In 1.0 ppm dose group gangrenous
dermatitis of tail and facial and podal dermatitis with mortality of 12.0% were also noticed. Significant
haematobiochemical observations included anaemia, leucopaenia, lymphocytopaenia, thrombocytopenia,
hypoproteinemia with decreased albumin: globulin ratios, hypoglycaemia and increased serum ALT, AST
and LDH activities, and increase in BUN and serum creatinine levels. Significant reduction in IgG, IgM,
IgA levels, HA titres against SRBCs, DTH with ovalbumin, amount of NO production by resident
peritoneal macrophages, SI indices, number of CD4+ and CD8+ and CD4+: CD8+ ratios in peripheral blood
and down regulation of different cytokines like IFN- ?, IL-2 and IL-4 and upregulation of IL-10 were
recorded in T-2 treated rats suggested suppression of AMI and CMI due to T-2 toxicity. Significant
increase in the MDA levels with decrease in SOD, catalase and GSH levels in kidneys, liver, brain, testes
and spleen indicated cell injury in T-2 toxicity due to free radical induced oxidative stress. Grossly,
kidneys and livers were pale and enlarged and spleen, thymus and testes were atrophic in T-2 treated
animals. Histopathologically, most consistent lesions included swollen and vacuolated epithelial cells of
PCTs with occasional necrosis and presence of proteinaceous and cellular casts in the lumen, congestion
of intertubular blood vessels, mononuclear cells infiltration in interstitium, swollen parietal epithelial cells
of Bowman’s capsule and dilatation of DCTs in kidneys; swollen hepatocytes with granular or vacuolated
cytoplasm, karyomegaly, double nuclei with anisokaryosis, proliferation of bile ductules and mononuclear
cell infiltration in the portal areas in liver; engorged blood vessels, haemorrhages, degeneration and
thining of muscle fibres with increased inter fascicular spaces in heart; engorgement of blood vessels
with increased perivascular spaces, occasional perivascular cuffing, increased perineuronal spaces and
focal haemorrhages and gliosis in cerebrum, severe degeneration and depletion of Purkinje cells in
cerebellum; lymphoid cells depletion and presence of large number of multinucleated megakaryocytes in
spleen; lymphoid cells depletion, lymphocytolysis, congestion and hemorrhage in interfollicular spaces,
extensive proliferation of interfollicular connective tissue causing atrophy in thymus; lymphoid cells
depletion in Peyer’s patches; degeneration and disorganization of spermatogonial cells with reduced
spermatogenesis in testes; reduced number of spermatozoa in epididymal ductules and extensive
vacuolation and necrosis of cortical cells with presence of interstitial MNCs infiltration in adrenal cortices.
Fifty feed samples were analysed for T-2 toxin by TLC and spectrophotometry and by competitive ELISA.
Thirteen samples were found positive by ELISA only with T-2 levels 0.120 ppm to 0.235 ppm. Five T-2
negative samples were spiked with known amount (0.05-10μg/g) of T-2 toxin. The lowest detection limit
was found to be 0.5 μg/g for TLC and Spectrophotometry and 0.125 μg/g for ELISA. It was concluded
that T-2 toxin produced significant toxicopathological changes in a dose and duration dependent manner.
It was found to be nephrotoxic, hepatotoxic and immunosuppressive. The tissue damage was due to free
radical induced oxidative stress. ELISA was found to be more sensitive method for detecting T-2 toxin in
feed than TLC and spectrophotometry.

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