Ki67 expression in the cerebellum of dogs with distemper

Yarim M., Gulbahar M. Y., Guvenc T., Kabak Y. B., Karayigit M. Ö.

REVUE DE MEDECINE VETERINAIRE, vol.162, no.5, pp.246-251, 2011 (SCI-Expanded) identifier identifier

  • Publication Type: Article / Article
  • Volume: 162 Issue: 5
  • Publication Date: 2011
  • Journal Indexes: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Page Numbers: pp.246-251
  • Çukurova University Affiliated: No


As the canine distemper virus (CDV) induces demyelination in the central nervous system, partially due to losses of glial cells, the aim of the present study was to determine the Ki67 immunoreactivity in demyelinated regions from cerebellum of dogs with acute and chronic CDV infection. Cerebella from naturally infected dogs (n = 12) were routinely processed for histopathology and the observed lesions were conventionally classified as acute (n = 6) or chronic (n = 6) cases. Immunohistochemical analyses were performed in parallel for detecting the CDV antigen using a mouse anti-CDV monoclonal antibody and for evaluating the proliferation index using a rabbit anti-Ki67 polyclonal antibody. Histological and immunohistochemical findings were compared to healthy cerebellum controls (n = 6). Contrary to controls, cerebella from infected dogs exhibited demyelinated areas, often moderate to severe, in which the viral presence was confirmed. Regarding the demyelination percentage, no significant difference was found between acute and chronic cases. The glial Ki67 proliferation indexes were roughly similar in the 2 groups of infected dogs and were markedly higher than in controls whereas the mean Ki67 immunopositive glial cell counts were dramatically increased in chronically infected dogs compared to the controls or to the acutely affected dogs. These results show that the glial cell proliferation progresses with the same intensity in both acute and chronic cases, although the total number of Ki67 positive cells is higher in chronically infected dogs, suggesting that compensatory mechanisms for counteracting demyelination.