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Abstract
The aim of this study was to evaluate the probable prophylactic potential of concurrent thiamine supplementation against sulfur toxicities in adult sheep.
Therefore, a total number of nine apparently healthy adult female Balady sheep (8 months old and 25-30 kg B.W) were fed a balanced died containing 10% dry roughages with green fooder and water ad libitum. Animals were divided into 3 equal groups; the first received the diet mixed with 8g of elemental sulfur/kg (0.8%) which is equivalent to the double of the maximum tolerable dose in ruminants. The second group received the same sulfur concentration besides 250mg B1 /Kg diet (0. 025%) and the third group was kept as control. Feeding on this diet continued till 25-28 days where the three animals on high sulfur diet were in extremis at days 25, 26 and 28 post feeding At this point, blood was collected and all the experimental animals were necropsies.
The clinical signs of sulfur intoxicated animals began at the day 14 post intoxication and included slight loss of appetite. Five days later, there were anorexia and slight diarrhea. On day 24 of the experiment, these animals developed blindness, neck and shoulder tremors head pressing, ataxia then recumbency, Coma then death occurred on days 25, 26 and 28 of each of the three intoxicated ewes. Upon administration of B1, no clinical signs were observed throughout the experiment in the second group.
Hematologically, all the parameters of complete blood picture in both treated groups were within normal limits except for PCV which elevated in ewes when compared with O day or the control value linear and vertical comparison). Both serum CK and AST activities elevated significantly in both groups either when compared linearly with O day value or when compared with the last day value Blood CL, K, mg and Ph concentrations all were significantly increased in animals of both groups.,
Necropsy of the treated animals revealed congestion and hemorrhages of the meninges besided minute tan yellow areas in the cerebral cortex Moreover, both the liver, and kidneys exhibited pale irregular sport.
Histopathologically, the neural lesions in the first group were mostly in the cerebral cortex and to some extent in the cerebellar cortex; however, the brain stem appeared not affected. The cerebral cortex, particularly the deep laminae showed neuronal degeneration and necrosis of the neurons associated with neuropil spongiosis. Moreover, perineural and pericapillary edema were evident besides slight lymphocytic cuffs. Satellitosis, neuronophagia and slight focal gliosis were evident. The covering meninges showed congestion and focal hemorrhages. Malacic small cavities were noticed in addition to ballooning of myeline sheath at the junctional white matter besides demyelination and gliosis. The cerebellar Purkinje and granule cells were focally necrotic and depleted. The extraneural lesions were also dramatic, particularly in the liver and lungs. The hepatic lesions were in the form of periportal severe necrosis with occasional centrilobular fatty change. The portal triads were not affected. The lungs showed multifocal edema that complicated to serofibrinous pneumonia because of invaders. Large bronchi showed goblet cell phyerplasia and smaller ones showed epithelial necrosis and desquamation. The renal lesions consisted of tubular erythrocytic casts accompanied by toxic tubulonecrosis of the distal convoluted and medullary tubules. The myocardium showed mild focal vacuolation and segmental necrosis of some myocytes with early trials of regeneration. The spleen showed moderate –to- severe lymphocytic cell depletion and excessue erythropoiesis.
Regandy animals of the second group, the aforemention lesions were seen except for less severe and much more localized neural and extraneural lesions besides complete absence of the cerebellar changes which thought to the reason of absence of the clinical disease in this group.
Finally, it could be concluded that concurrent supplementation of thiamine (250 ppm) against excess sulfur intake (0.8%) has a limited prophylactic potential where it alleviated the clinical disease but did not totally prevent the microscopic lesions.