NEUROPATHOLOGY OF BOVINE HERPESVIRUS TYPE-5 (BHV-5) MENINGOENCEPHALITIS IN A RABBIT SEIZURE MODEL

The suitability of a rabbit seizure model for studying the neuropathog enesis of bovine herpesvirus type 5 (BHV-5) encephalitis was evaluated . Intranasal administration of BHV-5 (strain TX89) together with intra muscular administration of dexamethasone produced seizures in 70% of r abbits tested and meningo-encephalitis in 100%. Infectious BHV-5 was c onsistently isolated from the following sites: olfactory bulb; anterio r cortex, containing the frontal cortex, olfactory tract and anterior portion of the olfactory cortex; posterior cortex, containing the temp oral, parietal, piriform, entorhinal and occipital cortices; amygdala; hippocampus. Less frequently, BHV-5 was isolated from the midbrain an d diencephalon, the pens and medulla, the cerebellum, and the trigemin al ganglia. Rabbits similarly infected with the Cooper strain of bovin e herpesvirus type 1 showed no neurological signs or meningo-encephali tis, and virus was not recovered from the brain. The brains of BHV-5-i nfected rabbits showed neuronal degeneration, leptomeningitis, gliosis and perivascular cuffing, predominantly in the olfactory cortex (piri form and entorhinal cortices), amygdala and hippocampus. Mild lymphocy tic meningitis was seen in the olfactory bulb and focal lymphocytic in filtration was sometimes present in the medulla and cerebellum. BHV-5, specific antigens and nucleic acids were detected in the olfactory co rtex, amygdala and hippocampus by immunohistochemical methods and in-s itu hybridization. The results suggested that, after intranasal BHV-5 inoculation, the virus spread to the central nervous system via the ol factory and trigeminal pathways. The olfactory pathway was more suscep tible than the trigeminal pathway to neuropathogenic effects. (C) 1997 W.B. Saunders Company Limited.