Predominant Involvement of the Cerebellum in Guinea Pigs Infected with Bovine Spongiform Encephalopathy (BSE)

This study reports the experimental transmission of bovine spongiform encephalopathy (BSE) to guinea pigs and describes the cerebellar lesions in these animals. Guinea pigs were inoculated intracerebrally with 10% brain homogenates from BSE-affected cattle. These animals were designated as the first...

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Bibliographic Details
Published in:Journal of comparative pathology 2011-05, Vol.144 (4), p.269-276
Main Authors: Furuoka, H., Horiuchi, M., Yamakawa, Y., Sata, T.
Format: Article
Language:English
Subjects:
Animals
Atrophy
Bovine spongiform encephalopathy
Brain
Brain - metabolism
Brain - pathology
Brain stem
BSE
Cattle
Cerebellum
Cerebellum - metabolism
Cerebellum - pathology
Cortex
Creutzfeldt-Jakob disease
Deposits
Disease Models, Animal
Encephalopathy, Bovine Spongiform - metabolism
Encephalopathy, Bovine Spongiform - pathology
Encephalopathy, Bovine Spongiform - transmission
experimental transmission
Female
Gliosis
Gliosis - pathology
guinea pig
Guinea Pigs
Immunohistochemistry
Infection
Kuru
Neurodegeneration
Neurotransmission
Plaques
Prion protein
PrPSc Proteins - metabolism
Thalamus
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Summary:This study reports the experimental transmission of bovine spongiform encephalopathy (BSE) to guinea pigs and describes the cerebellar lesions in these animals. Guinea pigs were inoculated intracerebrally with 10% brain homogenates from BSE-affected cattle. These animals were designated as the first passage. Second and third passages were subsequently performed. All guinea pigs developed infection at each passage. The mean incubation period of the first passage was 370 days post-infection (dpi) and this decreased to 307 dpi and 309 dpi for the second and third passages, respectively. Mild to severe spongiform degeneration and gliosis were observed in the cerebral cortex, thalamus and brainstem. In addition, the affected animals had marked pathological changes in the cerebellum characterized by severe cortical atrophy associated with Bergmann radial gliosis of the molecular layer and reduction in the width of the granular cell layer. Immunohistochemically, intense PrP Sc deposition and scattered plaque-like deposits were observed in the molecular and granular cell layers. Cerebellar lesions associated with severe atrophy of the cortex have not been reported in animal prion diseases, including in the experimental transmission of PrP Sc to small rodents. These lesions were similar to the lesions of human kuru or the VV2 variant of sporadic Creutzfeldt–Jakob disease, although typical kuru plaques or florid plaques were not observed in the affected animals.
ISSN:0021-9975
1532-3129
DOI:10.1016/j.jcpa.2010.10.004