The aim of the study was to evaluate the polioencephalomalacia induced with amprolium in goats: pathologic changes of the central nervous system. Eight apparently healthy goats of 6 to 9 weeks of age were drenched with amprolium (200 mg/kg body weight) till the development of clinical signs. Three goats of the same age group were drenched with tap water only and these served as controls. Amprolium drenched goats were allowed to die after the onset of clinical signs and control goats were euthanised after the death of amprolium fed goats. At the time of development of typical clinical signs of cerebrocortical necrosis (CCN) the goats were killed and necropsied and a complete histopathologic examination was performed. At necropsy of the four goats, large necrotic lesion was found in the cerebral cortex, and tissue thiamine levels decreased significantly, especially in cerebrum and cerebellum. However, the brain as a whole in all experimental animals, exhibited moderate to severe congestion, oedema and numerous small yellowish foci of varying sizes scattered on the surface of the cerebral hemispheres.Microscopic changes in the brain were limited to gray matter structures of cerebral and cerebellar cortex, caudal colliculi of mid brain, thalamus, cerebellum and spinal cord. There was shrinkage of neurons, perivascular and pericellular edema, necrosis of neurons, satellitosis, glial nodule, gliosis, middle laminar necrosis and deep laminar edema. Blood vessel walls were thickened due to hypertrophy and hyperplasia of endothelial and adventitial cells. Swollen and prominent capillary epithelium, satellitosis, presence of ghost cells, gliosis and perivascular cuffing were also observed but only in some of the animals. In the cerebellar cortex, there was degeneration of Purkinje cells. The caudal colliculi of mid brain showed bilateral malacia. To the best of our knowledge, these researchers questioned the hypothesis that the amprolium could be the major factor causing polioencephalomalacia. This is the first documentation of Amprolium-Induced cerebrocortical necrosis on goat in Iran.
Published in | American Journal of Internal Medicine (Volume 2, Issue 4) |
DOI | 10.11648/j.ajim.20140204.13 |
Page(s) | 67-71 |
Creative Commons |
This is an Open Access article, distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution and reproduction in any medium or format, provided the original work is properly cited. |
Copyright |
Copyright © The Author(s), 2014. Published by Science Publishing Group |
Polioencephalomalacia, Amprolium, Goat, Histopathology, Brain
[1] | Matayoshi M, Tsuha O, Shimoji S, Araki M, Uchihara T, Arakaki T, Ozawa T.Occurrence of cerebrocortical necrosis in a goat in Okinawa prefecture, Japan.J Vet Med Sci 2012; 74(9):1199-201. |
[2] | Ungerfeld EM, Rust SR, Burnett R. The effects of thiamine inhibition on ruminal fermentation: a preliminary study.Folia Microbiol (Praha) 2009; 54(6):521-6. |
[3] | Allen AL, Goupil BA, Valentine BA.A retrospective study of brain lesions in goats submitted to three veterinary diagnostic laboratories. J Vet Diagn Invest 2013; 25(4):482-9. |
[4] | Drewnoski ME, Ensley SM, Beitz DC, Schoonmaker JP, Loy DD.Assessment of ruminal hydrogen sulfide or urine thiosulfate as diagnostic tools for sulfur induced polioencephalomalacia in cattle.J Vet Diagn Invest. 2012; 24(4):702-9. |
[5] | Scott PR.Diagnosis and treatment of coenurosis in sheep.Vet Parasitol. 2012 ;189(1):75-8 |
[6] | Sakhaee E, Derakhshanfar A.Polioencephalomalacia associated with closantel overdosage in a goat.J S Afr Vet Assoc. 2010; 81(2):116-7. |
[7] | Javanbakht J, Hobbenaghi R, Hosseini E, Bahrami AM. Histopathological investigations of neuroprotective effects of Nigella sativa on motor neurons anterior horn spinal cord after sciatic nerve crush in rats. Pathol Biol (Paris). 2013 ;61(6):250-3 |
[8] | Hobbenaghi R, Javanbakht J, Sadeghzadeh Sh, Kheradmand D, Abdi FS.Neuroprotective effects of Nigella sativa extract on cell death in hippocampal neurons following experimental global cerebral ischemia-reperfusion injury in rats.J Neurol Sci 2014; 337(1-2):74-9. |
[9] | Bizon-Zygmańska D, Jankowska-Kulawy A, Bielarczyk H, Pawełczyk T.Acetyl-CoA metabolism in amprolium-evoked thiamine pyrophosphate deficits in cholinergic SN56 neuroblastoma cells. Neurochem Int 2011; 59(2):208-16. |
[10] | Iqbal A, Tariq KA, Wazir VS, Singh R. Antiparasitic efficacy of Artemisia absinthium, toltrazuril and amprolium against intestinal coccidiosis in goats. J Parasit Dis. 2013; 37(1):88-93. |
[11] | Ke ZJ, Wang X, Fan Z, Luo J. Ethanol promotes thiamine deficiency-induced neuronal death: involvement of double-stranded RNA-activated protein kinase.Alcohol Clin Exp Res 2009;33(6):1097-103 |
[12] | Parkhomenko IuM, Strokina AA, Pilipchuk SIu, Stepanenko SP.[Existence of two different active sites on thiamine binding protein in plasma membranes of synaptosomes].Ukr Biokhim Zh 2010;82(1):34-4 |
[13] | Amat S, McKinnon JJ, Olkowski AA, Penner GB, Simko E. Understanding the role of sulfur-thiamine interaction in the pathogenesis of sulfur-induced polioencephalomalacia in beef cattle. Res Vet Sci 2013; 95(3):1081-7. |
[14] | Cooper JJ, Schatzberg SJ, Vernau KM, Summers BA, Porter BF.Necrotizing meningoencephalitis in atypical dog breeds: a case series and literature review.J Vet Intern Med. 2014; 28(1):198-203. |
[15] | Krishnamoorthy P, Vairamuthu S, Balchandran C, Muralimanoha B. Pathology of chlorpyriphos and T-2 toxin in broiler chicken. Vet. Arhiv 2007; 77:47-57. |
[16] | Malik G, Dhahiya JP, Sandeep G, Mishra SK. Clinicopathological studies on chlorpyriphos intoxication in broiler chicken. Proceedings of 19th Annual Conference of Indian Association of Veterinary Pathologists. Palampur, India. 2008:124. |
[17] | Yadav SS, Mukhopadhayay SK, Purohit K. Experimentally induced chlorpyriphos toxicity in broilers: Haematobiochemical and pathomorphological studies. Proceedings of 20th Annual Conference of Indian Association of Veterinary Pathologists, 12- 14 November. Jabalpur, India. 2011:103. |
[18] | Goyal S, Rajinder HS, Sandhu SB.Histopathological alterations induced after oral sub-acute thiacloprid toxicity in Gallus domesticus. Veterinarski Arhiv 2010; 80(5):673-682. |
APA Style
Reza Sedaghat, Javad Javanbakht. (2014). Neurohistopathological Findings of the Effects of Amprolium on the Brain and Spinal Cord Changes in the a Animal Model: An Experimental Study. American Journal of Internal Medicine, 2(4), 67-71. https://doi.org/10.11648/j.ajim.20140204.13
ACS Style
Reza Sedaghat; Javad Javanbakht. Neurohistopathological Findings of the Effects of Amprolium on the Brain and Spinal Cord Changes in the a Animal Model: An Experimental Study. Am. J. Intern. Med. 2014, 2(4), 67-71. doi: 10.11648/j.ajim.20140204.13
@article{10.11648/j.ajim.20140204.13, author = {Reza Sedaghat and Javad Javanbakht}, title = {Neurohistopathological Findings of the Effects of Amprolium on the Brain and Spinal Cord Changes in the a Animal Model: An Experimental Study}, journal = {American Journal of Internal Medicine}, volume = {2}, number = {4}, pages = {67-71}, doi = {10.11648/j.ajim.20140204.13}, url = {https://doi.org/10.11648/j.ajim.20140204.13}, eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.ajim.20140204.13}, abstract = {The aim of the study was to evaluate the polioencephalomalacia induced with amprolium in goats: pathologic changes of the central nervous system. Eight apparently healthy goats of 6 to 9 weeks of age were drenched with amprolium (200 mg/kg body weight) till the development of clinical signs. Three goats of the same age group were drenched with tap water only and these served as controls. Amprolium drenched goats were allowed to die after the onset of clinical signs and control goats were euthanised after the death of amprolium fed goats. At the time of development of typical clinical signs of cerebrocortical necrosis (CCN) the goats were killed and necropsied and a complete histopathologic examination was performed. At necropsy of the four goats, large necrotic lesion was found in the cerebral cortex, and tissue thiamine levels decreased significantly, especially in cerebrum and cerebellum. However, the brain as a whole in all experimental animals, exhibited moderate to severe congestion, oedema and numerous small yellowish foci of varying sizes scattered on the surface of the cerebral hemispheres.Microscopic changes in the brain were limited to gray matter structures of cerebral and cerebellar cortex, caudal colliculi of mid brain, thalamus, cerebellum and spinal cord. There was shrinkage of neurons, perivascular and pericellular edema, necrosis of neurons, satellitosis, glial nodule, gliosis, middle laminar necrosis and deep laminar edema. Blood vessel walls were thickened due to hypertrophy and hyperplasia of endothelial and adventitial cells. Swollen and prominent capillary epithelium, satellitosis, presence of ghost cells, gliosis and perivascular cuffing were also observed but only in some of the animals. In the cerebellar cortex, there was degeneration of Purkinje cells. The caudal colliculi of mid brain showed bilateral malacia. To the best of our knowledge, these researchers questioned the hypothesis that the amprolium could be the major factor causing polioencephalomalacia. This is the first documentation of Amprolium-Induced cerebrocortical necrosis on goat in Iran.}, year = {2014} }
TY - JOUR T1 - Neurohistopathological Findings of the Effects of Amprolium on the Brain and Spinal Cord Changes in the a Animal Model: An Experimental Study AU - Reza Sedaghat AU - Javad Javanbakht Y1 - 2014/07/30 PY - 2014 N1 - https://doi.org/10.11648/j.ajim.20140204.13 DO - 10.11648/j.ajim.20140204.13 T2 - American Journal of Internal Medicine JF - American Journal of Internal Medicine JO - American Journal of Internal Medicine SP - 67 EP - 71 PB - Science Publishing Group SN - 2330-4324 UR - https://doi.org/10.11648/j.ajim.20140204.13 AB - The aim of the study was to evaluate the polioencephalomalacia induced with amprolium in goats: pathologic changes of the central nervous system. Eight apparently healthy goats of 6 to 9 weeks of age were drenched with amprolium (200 mg/kg body weight) till the development of clinical signs. Three goats of the same age group were drenched with tap water only and these served as controls. Amprolium drenched goats were allowed to die after the onset of clinical signs and control goats were euthanised after the death of amprolium fed goats. At the time of development of typical clinical signs of cerebrocortical necrosis (CCN) the goats were killed and necropsied and a complete histopathologic examination was performed. At necropsy of the four goats, large necrotic lesion was found in the cerebral cortex, and tissue thiamine levels decreased significantly, especially in cerebrum and cerebellum. However, the brain as a whole in all experimental animals, exhibited moderate to severe congestion, oedema and numerous small yellowish foci of varying sizes scattered on the surface of the cerebral hemispheres.Microscopic changes in the brain were limited to gray matter structures of cerebral and cerebellar cortex, caudal colliculi of mid brain, thalamus, cerebellum and spinal cord. There was shrinkage of neurons, perivascular and pericellular edema, necrosis of neurons, satellitosis, glial nodule, gliosis, middle laminar necrosis and deep laminar edema. Blood vessel walls were thickened due to hypertrophy and hyperplasia of endothelial and adventitial cells. Swollen and prominent capillary epithelium, satellitosis, presence of ghost cells, gliosis and perivascular cuffing were also observed but only in some of the animals. In the cerebellar cortex, there was degeneration of Purkinje cells. The caudal colliculi of mid brain showed bilateral malacia. To the best of our knowledge, these researchers questioned the hypothesis that the amprolium could be the major factor causing polioencephalomalacia. This is the first documentation of Amprolium-Induced cerebrocortical necrosis on goat in Iran. VL - 2 IS - 4 ER -