“West Nile Virus outbreak in italy: pathological findings in two horses”

none7The aim of this presentation is to describe the gross and histological findings in two horses affected by West Nile Disease (WND) examined during the WND outbreak which occurred in Italy in the 2008 late summer. Both horses had been euthanized for humane reasons because of the severity of neurological signs. Complete postmortem examination was carried out immediately after euthanasia. Representative tissue samples of the CNS and major organs were fixed in 10% buffered formalin, processed for histology and stained with hematoxylin and eosin, periodic acid-Schiff, Luxol Fast blue and cresyl violet. Furthermore, samples of fresh CNS tissue were collected for virology. The first horse was a 7-year-old female Selle Français with severe tetraparesis, mild changes in mental status and cranial nerves and permanent recumbency. Gross lesions were limited to the spinal cord; multifocal pinpoint hemorrhages were evident especially in the thoracic and lumbar tracts; in the lumbosacral segments the gray matter showed an asymmetric discoloration of the ventral horns, associated with haemorrhagic infarction. Histologically, inflammatory and degenerative lesions suggestive of viral infection were evident in all the CNS tracts (brain and spinal cord). Notably, cerebral cortex, diencephalon and brain stem showed multifocal perivascular cuffs formed almost exclusively by small lymphocytes and at lesser extent by histiocytes and small foci of hemorrhages; capillaries lumina were dilated and hyperemic. The neuropil showed marked neuronal degeneration, chromatolysis and cell shrinkage; there were also multifocal microglial nodules, containing rare neutrophils admixed with glial cells. The spinal cord prompted a pattern of degenerative and inflammatory changes similar to those detected in the brain neuropil, being the thoracic tract the most severely affected: chromatolysis, cell shrinkage, neuronophagia and lymphocytic perivascular cuffing were evident in the gray matter; furthermore, there were foci of extravasated erythrocytes dissecting myelin fibers in the white matter, and frequent axonal swellings (spheroid formation). The diagnosis was severe, subacute, multifocal, not suppurative polyoencephalomyelitis. RT-PCR from CNS samples was positive for WND virus. The second horse was a 19-year-old Appaloosa gelding with severe tetraparesis. Post mortem examination demonstrated multifocal pinpoint hemorrhages in the gray matter of thoracic spinal cord segments. The skull opening revealed some white, compact, nodular thickenings of the dura mater, ranging from 1 to 5 mm in diameter, similar to the age-related Pacchioni collagen granulations. In the extraneural tissues there were signs of moderate cardio-respiratory insufficiency. At histology, thoracic tracts of the spinal cord showed multifocal perivascular hemorrhages and focal influx of lymphocytes within the gray matter. The histological diagnosis was mild, focal poliomyelitis and multifocal spinal hemorrhages. CNS samples were positive for WND virus. In both horses the histological lesions were suggestive of viral encephalomyelitis, and the role of WNDV was confirmed by molecular analysis. The different clinical presentation, showing intracranial involvement only in one horse, was confirmed on neuropatholologic examination. In the first case, the changes were distributed in both the brain and the spinal cord, while in the second horse only the spinal cord was affected histologically. Noteworthy, this different pattern did not match the severity of neurological signs. These findings confirm the observations from others, as for the prevalence of spinal cord lesions in WND, as for the poor correlation between the severity of clinical and histological signs. Beside the inflammatory infiltrate, the likely basis of neurological symptoms relies on the neuronal degenerative changes; however, it is still uncertain if these changes are triggered by neurotropic cytopathic...Comunicazione orale 26/09/2009mixedL. Mandrioli; G. Bettini; M. Morini; A. Gallucci; R Biserni; A. Spadari; G. GandiniL. Mandrioli; G. Bettini; M. Morini; A. Gallucci; R Biserni; A. Spadari; G. Gandin