Dogs aged 20 to 210 days were inoculated intracerebrally with Japanese B encephalitis virus, G1 strain, of the 242nd to 247th mouse brain passages. Twelve out of the 17 inoculated dogs developed recognizable signs after incubation periods of 2 to 13 days. Major signs manifested were poor appetite and ataxia. Distinct ataxia was accompanied usually by general prostration. Trismus, tic, tremor, or flaccid paresis were also observed, whereas nuchal rigidity and generalized spasticity were not seen. Active virus was re-isolated from brain tissues of infected dogs, and was identified as Japanese B encephalitis by neutralization tests. Increase of the original virus in brain tissues was demonstrated. Histologically, cell infiltration, glial proliferation, destruction of nerve cells, and formation of necrotic foci were noted in the central nervous system. The cell infiltration and glial proliferation occurred disseminatedly in the whole brain and spinal cord, affecting severely both the gray and white matters. Perivascular cuffs or sleeves were commonly found. The destruction of nerve cells took place also ubiquitously. Nerve cell involvement was varied in type: simple or severe chromatolysis, pycnosis, shrinkage of cell body or neuronophagia. These alterations developed most markedly in the thalamus. The necrotic foci were confined to the white matter, usually lacking in marked cellular response. In these foci the axis cylinders were severely destroyed. Focal swelling of leptomeninges and cellular exudation into the central canal and ventricles were also noted. Comparison of the canine infection with human Japanese B encephalitis is discussed.