The pathologic and peroxidase immunohistochemical features of West Nile flavivirus (WNV) infection were compared in four horses from the northeastern United States and six horses from central Italy. In all 10 animals, there were mild to severe polioencephalomyelitis with small T lymphocyte and lesser macrophage perivascular infiltrate, multifocal glial nodules, neutrophils, and occasional neuronophagia. Perivascular hemorrhages, also noted macroscopically in two animals, were observed in 50% of the horses. In the four American horses, lesions extended from the basal nuclei through the brain stem and to the sacral spinal cord and were more severe than the lesions observed in the six Italian horses, which had moderate to severe lesions mainly in the thoracolumbar spinal cord and mild rhombencephalic lesions. WNV antigen was scant and was identified within the cytoplasm of a few neurons, fibers, glial cells, and macrophages. WNV infection in horses is characterized by lesions with little associated antigen when compared with WNV infection in birds and some fatal human infections and with other important viral encephalitides of horses, such as alphavirus infections and rabies.

Natural eastern equine encephalitis alphavirus (EEEV) infection was diagnosed in two adult horses with anorexia and colic, changes in sensorium, hyperexcitability, and terminal severe depression. Myocardium, tunica muscularis of stomach, intestine, urinary bladder, and spleen capsule had coagulative necrosis and perivascular lymphocytic infiltrate. Central nervous system (CNS) lesions were diffuse polioencephalomyelitis with leptomeningitis characterized by perivascular T lymphocyte cuffing, marked gliosis, neuronophagia, and multifocal microabscesses. Lesions were more prominent within cerebral cortex, thalamus, hypothalamus, and mesencephalon. EEEV was identified in the cytoplasm of cardiac myocytes and smooth muscle cells of spleen, stomach, intestine, urinary bladder, blood vessels, and dendritic cells. In the CNS, EEEV-positive cells included neurons, astrocytes, oligodendrocytes, microglia, and neutrophils. EEEV was isolated from the CNS of both horses. The detailed description of the encephalic and spinal EEEV localization and the findings of EEEV in extraneural tissues contribute to the understanding of this important multisystemic zoonotic disease.

A 4-year-old male Pekingese dog was referred to the clinic with a history of recurrent seizures and progressive abnormal gait and behavior, which did not respond to treatment. At necropsy, a large cortical defect in the right temporo-parietal cortex, malacia of subcortical white matter, right basal nuclei, and capsula interna, as well as abnormalities of the right hippocampus were observed. Histological examination of the brain revealed moderate to severe nonsuppurative meningoencephalitis in the left cerebral hemisphere and extensive infarction-like lesions with milder inflammation in the right hemisphere. In the right hippocampus, the pyramidal cells were arranged in a gyrus-like pattern and intermingled with gemistocytic and fibrillary astrocytes. The histopathological features of the inflammatory lesions were consistent with necrotizing meningoencephalitis and resembled those described in so-called Pug dog encephalitis. The hippocampal changes were interpreted as dysplasia (monolateral hippocampal cortical hamartia), unrelated to clinical signs and necrotizing inflammatory lesions.