Intratracheal inoculation of 2-week old quail chicks with Aspergillus flavus spores resulted in the development of clinical signs within 24 h of infection. These were characterized by dullness, depression, anorexia, accelerated breathing, gasping and prostration leading to death. These signs continued up to 7 days followed by considerable decrease in the intensity of the symptoms as well as number of birds showing clinical signs. Mortality occurred primarily in the first week with a majority of the birds dying from 2-4 days after infection. The overall mortality during a 6-week observation period was 25%. The average body weight of the infected chicks was slightly lower than that of controls; the difference being significant at 2, 3 and 42 days post-infection. There was no appreciable difference in the mean values of haemoglobin, packed cell volume and total erythrocyte count between the infected and control chicks at any stage of infection, but total leucocyte count revealed a significant increase (p less than 0.05) from 3-7 days post-infection. This was due to increase in the percentage of heterophils and decrease in lymphocytes.

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Feeding of aflatoxin B1 @ 1 ppm to 2-week old Japanese quail for a period of 8 weeks produced gross and microscopic changes in the liver, skeletal muscles, heart and bursa of Fabricius. These included fatty changes, bile duct hyperplasia and lymphoid aggregation in liver; haemorrhages in thigh, breast muscles and myocardium; mild depletion of lymphocytes, cystic degeneration and fibrous tissue proliferation in bursa of Fabricius. More or less similar lesions were seen in quail chicks fed on aflatoxin with sodium selenite @ 5 ppm but these were of lesser intensity and appeared at later stages of the experiment thereby indicating that supplementation of selenium had some protective action against the toxic effect of aflatoxin B1 in Japanese quail.

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Summary Eight apparently healthy male buffalo calves of 6 to 12 months of age were drenched with amprolium*** (300 mg/kg body weight) till the development of clinical signs. Four buffalo calves of the same age group were drenched with tap water only and these served as controls. Amprolium drenched calves were allowed to die after the onset of clinical signs and control calves were euthanised after the death of amprolium fed calves. Tissues were collected for histopathological studies. Formalin fixed brain slices were examined for autofluorescence with the help of ultraviolet light at 365 nm. Gross and histopathological changes were mainly confined to the brain in amprolium fed calves. Gross lesions included congestion and haemorrhages in the meninges. The cerebral gyri were swollen with yellowish discolouration of cerebral cortex. Microscopic changes in the brain were limited to gray matter structures of cerebral and cerebellar cortex, caudal colliculi of mid brain and thalamus. There was shrinkage of neurons, perivascular and pericellular edema, necrosis of neurons, satellitosis, glial nodule and gliosis. Blood vessel walls were thickened due to hypertrophy and hyperplasia of endothelial and adventitial cells. In the cerebellar cortex, there was degeneration of Purkinje cells. The caudal colliculi of mid brain showed bilateral malacia. In the necrotic areas, neuropils were fragmented, edematous and hypercellular due to increased number of microglial cells and there was neocapillary formation. Subcortical gray matter of the thalamus showed necrosis of neurons, gliosis with formation of glial nodule. Formalin‐fixed brain slices of amprolium fed calves showed disseminated areas of greenish yellow autofluorescence in the cerebral cortex when viewed under ultraviolet light at 365 nm.

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