Immunophenotyping of Granulomatous Meningoencephalitis in 4 Dogs
ACVIM 2008
K.M. Vernau; W. Vernau; R.A. LeCouteur; R.J. Higgins; B.K. Sturges; P.J. Dickinson; D.R. Westworth; D.K. Naydan; P.F. Moore
School of Veterinary Medicine, University of California
Davis, CA, USA

Granulomatous meningoencephalomyelitis (GME) is a devastating idiopathic inflammatory disease affecting the CNS of dogs. Definitive diagnosis is based on characteristic histopathological findings. A previous study assessed formalin-fixed brain from dogs with GME using a restricted panel of reagents. Lesions consisted of a mixture of macrophages and lymphocytes, with a predominance of T and few B lymphocytes. The purpose of this study is to further elucidate the pathogenesis of GME by more fully characterizing the inflammatory cells in the brains of dogs with GME.

Four dogs with histopathologically confirmed GME were identified. A complete necropsy was done in all dogs. Based on MRI, sections of fresh brain lesions were frozen in OCT medium and adjacent sections immersion-fixed in 10% neutral buffered formalin. Immunophenotyping of inflammatory cell infiltrates was done on both formalin-fixed and adjacent fresh frozen brain sections, using panels of antibodies specific for canine leukocyte markers.

In all dogs, immunophenotyping demonstrated that perivascular cuffs in the parenchyma contained a mixed population of inflammatory cells, with lymphocytes, macrophages, dendritic cells and plasma cells predominating. B lymphocytes accounted for the majority of lymphocytes with lesser numbers of a mixture of CD4+ and CD8+ T lymphocytes. Macrophages and dendritic cells were activated as evidenced by upregulation of CD4 and CD80, and CD80 and CD86 expression respectively. In the brain parenchyma and meninges was a similar but less severe inflammatory infiltrate. These data suggest that a viral etiology is unlikely and that humoral immunity plays a major role in the pathogenesis of GME.

Speaker Information
(click the speaker's name to view other papers and abstracts submitted by this speaker)

Karen Vernau


MAIN : SA Neurology : Granulomatous Meningoencephalitis
Powered By VIN
SAID=27