An 11-year-old spayed female Beagle canine suffered from a sudden onset of ataxia, blindness and died 10 hours later. Results of radiographic analysis, complete blood count, and blood chemistry profile were within normal limits. Full necropsy was performed. Grossly, severe congestion was observed in the brain, spinal cord, lungs, spleen and heart. Histopathologically, there was severe multifocal to coalescing lymphoplasmacytic and histiocytic necrotizing vasculitis in the brain and spinal cord while no remarkable lesions were noted in any other organ system. To identify possible infectious agents, periodic acid-Schiff (PAS), Gomori (GMS) and Gram staining were performed, and none demonstrated any organism. Immunohistochemistry for canine distemper virus (CDV) was also negative. Characterization of the inflammatory cell subtypes within the central nervous system lesions was performed using immunohistochemistry. There was marked positive immunoreactivity for CD3 observed primarily in the cytoplasm of intralesional lymphocytes demonstrating that the predominant population were T-cell lymphocytes. The inflammatory cells were negative for PAX5 antibody. Based on histopathologic and immunohistochemical investigation, the tentative diagnosis is an immune-mediated encephalomyelitis which can be differentiated as either granulomatous meningoencephalitis or canine juvenile polyarteritis syndrome (Beagle pain syndrome). The objective of this study was to describe the subtype of inflammatory cells within the vascular lesions of this immune-mediated encephalomyelitis in a Beagle.