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- Selective Neuronal Damage Produced by beta-fluoroethylacetate Intoxication in Rat Brain.
- Ki Hyeong Lee, Beom Seok Jeon, Duk Lyul Na, Seong Ho Park, Je G Chi
- Korean J Pathol. 1995;29(3):277-285.
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Abstract
PDF - Beta-fluoroethylacetate has been extensively used as the rodenticide in Korea. In some patients with acute poisoning, beta-fluoroethylacetate caused cerebellar dysfunction as a single and persistent neurologic sequela after a period of an acute neurological disorder which is characterized by mental deterioration, seizures, and respiratory failure. But there has been no report of pathological findings to explain neurological deficit. We tried to verify the histologic changes of the central nervous systems in beta-fluoroethylacetate poisoned rats. Silver staining(Gallyas) was used to evaluate the histology. In acute intoxication experiment with LD50(7mg/Kg), beta-fluoroethylacetate elicited acute onset of consciousness deterioration, generalized tonic-clonic seizures and large amplitude tremulous activity involving whole body with full recovery after 24 hours. There was no discernible pathologic change in CNS in acutely poisoned rats. However, when poisoned with sublethal dose(5mg/Kg) daily for five days, a moderate degree of nerve cell degeneration was found selectively in dentate nucleus, Purkinie cell layer, vestibulo-cochlear nucleus and striatum. This change was not seen in hippocampus, cerebral cortex or cerebellar cortex. These findings were well correlated with the previous reports of selective pathology in human 5-FU intoxication cases. Our preliminary results suggest that beta-fluoroethylacetate, a kind of cellular metabolism inhibitor may induce selective neuropathology mainly involving cerebellar output pathway in rats.
- Negri Bodies in Rabid Dog: Light and Electron Microscopic Findings.
- Eon Sub Park, Young Uk Park, Jae Hyung Yoo, Kye Yong Song, Je G Chi
- Korean J Pathol. 1992;26(6):615-619.
- 3,003 View
- 66 Download
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Abstract
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- Rabies is a fetal viral encephalitis to which all mammals, including man are susceptible. This virus, the genus of Rhabdovirus, is usually present in the saliva of infected animals and is transmitted by their bite. As a rule the virus enter the CNS by ascending along peripheral nervous system and extremely variable in extent. Negri bodies are appear in about 75% of cases. These bodies are eosinophilic, usually rounded inclusions and is located in the cystoplasm of the neurons, most frequently in the pyramidal neurons of the Hippocampus and the Purkinje cells of the cerebellum. We have experienced a case of canine rabies that showed Negri bodies in the Purkinje cells along with diffuse degenerative encephalitis and perivascular mononuclear cells infiltration. The Negri bodies were best demonstrated by Negri body staining although routine H-E staind was also useful. There inclusion bodies were located exclusively in the cytoplasm, and were found occasionally. Electron microscopic findings of the Negri bodies showed aggregates of bulletshaped nucleocapsids. We report a Negri body found in the brain of rabid dog with the light and electron microscopic findings.
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