Brain lesions associated with acute toxic hepatopathy in cattle

Samples of the liver, telencephalon, brainstem, and cerebellum were obtained from 22 bovids suffering from spontaneous or experimental acute toxic liver disease. Perreyia flavipes larvae, and leaves of Cestrum corymbosum, Cestrum intermedium, Dodonaea viscosa, Trema micrantha, and Xanthium cavanille...

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Bibliographic Details
Published in:Journal of veterinary diagnostic investigation 2017-05, Vol.29 (3), p.287-292
Main Authors: Wouters, Angelica T. B., Wouters, Flademir, Boabaid, Fabiana M., Watanabe, Tatiane T. N., Fredo, Gabriela, Varaschin, Mary S., Driemeier, David
Format: Article
Language:English
Subjects:
Animals
Astrocytes - cytology
Brain - metabolism
Cattle
Cattle Diseases - diagnosis
Cattle Diseases - metabolism
Cattle Diseases - pathology
Cerebellum - metabolism
Chemical and Drug Induced Liver Injury - diagnosis
Chemical and Drug Induced Liver Injury - veterinary
Glial Fibrillary Acidic Protein - metabolism
Immunohistochemistry - veterinary
Liver - metabolism
Staining and Labeling
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Summary:Samples of the liver, telencephalon, brainstem, and cerebellum were obtained from 22 bovids suffering from spontaneous or experimental acute toxic liver disease. Perreyia flavipes larvae, and leaves of Cestrum corymbosum, Cestrum intermedium, Dodonaea viscosa, Trema micrantha, and Xanthium cavanillesii were the causal agents in the disorders studied. Hematoxylin and eosin and periodic acid–Schiff staining, as well as anti-S100 protein (anti-S100), anti–glial fibrillary acidic protein (anti-GFAP), and anti-vimentin immunostaining were used to evaluate the brain sections. Astrocytic changes were observed in all samples and were characterized by swollen vesicular nuclei in gray (Alzheimer type II astrocytes) and white matter; and by abundant eosinophilic or vacuolated cytoplasm with pyknotic nuclei in the white matter. These changes were evidenced by anti-S100 and anti-GFAP immunostaining. Our study demonstrates major changes in astrocytes of cattle that died with neurologic clinical signs as the result of acute toxic liver disease.
ISSN:1040-6387
1943-4936
DOI:10.1177/1040638717699242