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Neuropathologic study of experimental classical swine fever
J C Gómez-Villamandos1, I García de Leániz, A Núñez
1Departamento de Anatomía y Anatomía Patológica Comparadas, Facultad de Veterinaria, Universidad de Córdoba, Edificio de Sanidad Animal, Campus de Rabanales, 14014, Córdoba (Spain). jcgomez@uco.es
Veterinary Pathology
|July 19, 2006
Summary
Classical swine fever (CSF) causes nonpurulent meningoencephalitis and lymphocyte apoptosis in the central nervous system (CNS). Viral infection is linked to apoptosis but not always to cell infiltrates or hemorrhages.
Area of Science:
- Veterinary Pathology
- Virology
- Neuroscience
Background:
- Classical swine fever (CSF) is a highly contagious viral disease affecting pigs.
- Understanding the pathogenesis of central nervous system (CNS) lesions in CSF is crucial for disease management.
Purpose of the Study:
- To characterize the spatial and chronologic distribution of CNS lesions and viral antigen in experimental CSF.
- To elucidate the pathogenetic mechanisms of CNS lesions and the role of the virus.
Main Methods:
- Experimental infection of 28 pigs with a virulent CSF virus isolate.
- Analysis of CNS tissues using immunohistochemistry, electron microscopy, and TUNEL assay.
- Evaluation of cellular infiltrates and apoptosis from 2 to 15 days postinoculation.
Main Results:
- Nonpurulent meningoencephalitis, microhemorrhages, and lymphocyte apoptosis were observed in the CNS.
- Early viral infection targeted lymphocytes and microglial cells, primarily in the rostral telencephalon.
- Apoptosis of infiltrating lymphocytes was temporally and spatially associated with viral infection, but the link to cell infiltrate presence was unclear. Macrophage involvement was minimal.
Conclusions:
- CSF induces specific inflammatory and degenerative lesions in the porcine CNS.
- Viral infection plays a role in lymphocyte apoptosis within CNS lesions.
- Further research is needed to clarify the relationship between viral infection and the inflammatory cell infiltrate in CSF-induced neuroinflammation.
