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Histopathological study of encephalomalacia in neonatal calves and application of neuronal and axonal degeneration marker
Five calves that had shown neurological symptoms within 9 days after birth were histopathologically diagnosed as encephalomalacia. Two calves showed bilateral laminar cerebrocortical necrosis and neuronal necrosis in the corpus striatum and hippocampus. Since the distributional pattern of the lesion...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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The Japanese Society of Veterinary Science
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6068296/ https://www.ncbi.nlm.nih.gov/pubmed/29731475 http://dx.doi.org/10.1292/jvms.18-0143 |
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author | KOYAMA, Kenji KANGAWA, Akihisa FUKUMOTO, Natsuko WATANABE, Ken-ichi HORIUCHI, Noriyuki OZAWA, Tomomi INOKUMA, Hisashi KOBAYASHI, Yoshiyasu |
author_facet | KOYAMA, Kenji KANGAWA, Akihisa FUKUMOTO, Natsuko WATANABE, Ken-ichi HORIUCHI, Noriyuki OZAWA, Tomomi INOKUMA, Hisashi KOBAYASHI, Yoshiyasu |
author_sort | KOYAMA, Kenji |
collection | PubMed |
description | Five calves that had shown neurological symptoms within 9 days after birth were histopathologically diagnosed as encephalomalacia. Two calves showed bilateral laminar cerebrocortical necrosis and neuronal necrosis in the corpus striatum and hippocampus. Since the distributional pattern of the lesions was consistent with that of global ischemia in other species, the lesions were probably hypoxic/ischemic encephalopathy consistent with the history of dystocia and perinatal asphyxia. One calf also showed bilateral laminar cerebrocortical necrosis. However, the lesions were chronic ones, because the calf had survived for long time and necropsied at postnatal day 118. Additionally, the lesions did not involve the corpus striatum and hippocampus. The other two calves showed multifocal necrosis with vascular lesions characterized by fibrin thrombi, perivascular edema and perivascular hyaline droplets in the cerebral cortex, corpus striatum, thalamus, brain stem and cerebellum. Considering the age of onsets and histopathological appearance, it was possible that latter three calves were also hypoxic/ischemic encephalopathy, however, exact cause of them was not revealed. In all calves, degenerated/necrotic neurons showed positive reactions for Fluoro-Jade C and degenerated axons showed immunoreactivity for Alzheimer precursor protein A4. Therefore, these markers were applicable to examination of brain injury in neonatal calves. |
format | Online Article Text |
id | pubmed-6068296 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | The Japanese Society of Veterinary Science |
record_format | MEDLINE/PubMed |
spelling | pubmed-60682962018-08-06 Histopathological study of encephalomalacia in neonatal calves and application of neuronal and axonal degeneration marker KOYAMA, Kenji KANGAWA, Akihisa FUKUMOTO, Natsuko WATANABE, Ken-ichi HORIUCHI, Noriyuki OZAWA, Tomomi INOKUMA, Hisashi KOBAYASHI, Yoshiyasu J Vet Med Sci Pathology Five calves that had shown neurological symptoms within 9 days after birth were histopathologically diagnosed as encephalomalacia. Two calves showed bilateral laminar cerebrocortical necrosis and neuronal necrosis in the corpus striatum and hippocampus. Since the distributional pattern of the lesions was consistent with that of global ischemia in other species, the lesions were probably hypoxic/ischemic encephalopathy consistent with the history of dystocia and perinatal asphyxia. One calf also showed bilateral laminar cerebrocortical necrosis. However, the lesions were chronic ones, because the calf had survived for long time and necropsied at postnatal day 118. Additionally, the lesions did not involve the corpus striatum and hippocampus. The other two calves showed multifocal necrosis with vascular lesions characterized by fibrin thrombi, perivascular edema and perivascular hyaline droplets in the cerebral cortex, corpus striatum, thalamus, brain stem and cerebellum. Considering the age of onsets and histopathological appearance, it was possible that latter three calves were also hypoxic/ischemic encephalopathy, however, exact cause of them was not revealed. In all calves, degenerated/necrotic neurons showed positive reactions for Fluoro-Jade C and degenerated axons showed immunoreactivity for Alzheimer precursor protein A4. Therefore, these markers were applicable to examination of brain injury in neonatal calves. The Japanese Society of Veterinary Science 2018-05-04 2018-07 /pmc/articles/PMC6068296/ /pubmed/29731475 http://dx.doi.org/10.1292/jvms.18-0143 Text en ©2018 The Japanese Society of Veterinary Science This is an open-access article distributed under the terms of the Creative Commons Attribution Non-Commercial No Derivatives (by-nc-nd) License. (CC-BY-NC-ND 4.0: https://creativecommons.org/licenses/by-nc-nd/4.0/) |
spellingShingle | Pathology KOYAMA, Kenji KANGAWA, Akihisa FUKUMOTO, Natsuko WATANABE, Ken-ichi HORIUCHI, Noriyuki OZAWA, Tomomi INOKUMA, Hisashi KOBAYASHI, Yoshiyasu Histopathological study of encephalomalacia in neonatal calves and application of neuronal and axonal degeneration marker |
title | Histopathological study of encephalomalacia in neonatal calves and application of neuronal and axonal degeneration marker |
title_full | Histopathological study of encephalomalacia in neonatal calves and application of neuronal and axonal degeneration marker |
title_fullStr | Histopathological study of encephalomalacia in neonatal calves and application of neuronal and axonal degeneration marker |
title_full_unstemmed | Histopathological study of encephalomalacia in neonatal calves and application of neuronal and axonal degeneration marker |
title_short | Histopathological study of encephalomalacia in neonatal calves and application of neuronal and axonal degeneration marker |
title_sort | histopathological study of encephalomalacia in neonatal calves and application of neuronal and axonal degeneration marker |
topic | Pathology |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6068296/ https://www.ncbi.nlm.nih.gov/pubmed/29731475 http://dx.doi.org/10.1292/jvms.18-0143 |
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