Texas Equine Veterinary Association

uncertain for N. hughesi, although it appears that foals can be infected by transplacental passage of the parasite. In many geographic areas of the Americas, S neurona infection is common, as evidenced by the proportion of horses exhibiting antibodies against the parasites. However, clinical disease is relatively uncommon (<1% of seropositive horses). Anticoccidial drugs will halt infection, but early diagnosis and treatment are critical to minimize immune-mediated damage to the central nervous system. Equine herpesvirus myeloencephalopathy (EHM), although an uncommon manifestation of equine herpesvirus-1 (EHV-1) infection, can cause devastating losses on individual farms, boarding stables, veterinary hospitals, and show and racing venues. Outbreaks of EHM have been recognized for centuries in domestic horse populations; many aspects of this disease remain poorly characterized. In recent years, an improved understanding of EHM has emerged from experimental studies and from data collected during field outbreaks at riding schools, racetracks, horse shows, and veterinary hospitals throughout North America and Europe. These outbreaks have highlighted the contagious nature of EHV-1 and have prompted a reevaluation of diagnostic procedures, treatment modalities, preventative measures, and biosecurity protocols for this disease. This current review article focuses on recent data related to the cause, epidemiology, pathogenesis, immunity, diagnosis, treatment, and prevention of EHV-1 infection with emphasis on EHM. Aside from EHV-1 a number of viruses transmitted by biological vectors or through direct contact, air, or ingestion cause neurologic disease in equids. Of interest are viruses of the Togaviridae, Flaviviridae, Rhabdoviridae, Herpesviridae, Bornaviridae, and Bunyaviridae families. Many are classified as arboviruses because they use arthropod vectors, whereas others are transmitted directly via ingestion, inhalation, or integument damage. They reach the central nervous system through blood, carried by mononuclear cells, or via retrograde axonal transport to the spinal cord or directly to the brain via the olfactory and nasopharyngeal epithelium. Lesions and clinical signs are the result of vascular damage, hemorrhage, thrombosis, edema, inflammation, neuronal and glial cell degeneration and dysfunction, apoptosis, and necrosis. Variable degree of inflammation is present with these viruses but lack of an inflammatory response does not rule out their presence. Equine degenerative myeloencephalopathy (EDM) is a progressive, symmetric disease of neuronal degeneration first described by (Mayhew, deLahunta, Whitlock) in a group of horses of mixed breeding in 1977. These horses were first observed to be ataxic before the age of 12 months. Neurologic deficits consisted of abnormal limb positioning, pelvic limb ataxia, thoracic limb hypermetria, and decreased strength and spasticity of the limbs and were characterized as upper motor neuron and general proprioceptive tract lesions. There was no evidence of cranial nerve, cerebral, or cerebellar involvement, and affected horses were clinically indistinguishable from those with other focal, multifocal, or diffuse myelopathies affecting the cervical spinal cord. Antemortem diagnostics included a routine hemogram, chemistry panel, urinalysis, cerebrospinal fluid (CSF) analysis, lateral radiographs, and a cervical venogram and myelogram under general anesthesia. Hematologic and biochemical values were within normal limits and there was no evidence of compression of the spinal cord at postmortem examination. Histologically, all animals had a diffuse degenerative myeloencephalopathy, with degeneration of the neuronal processes of the white matter of all spinal cord funiculi, especially in the dorsal spinocerebellar tract. Dystrophic axons were found at most spinal cord levels and were most severe in the nucleus of the dorsal spinocerebellar tract, especially in the thoracic segments (T10 to T15). Axonal dystrophy was also noted in the caudal medulla within the nucleus gracilis, medial cuneate nucleus and lateral (accessory) cuneate nucleus (LACN) and was most severe in the latter. Trauma to the nervous system in horses occurs through accidents that usually cause blunt force trauma and occasionally penetrating injuries. For nervous tissue damage to occur, skull or vertebral body fractures are not always necessary; however, careful evaluation for fractures of the skull and vertebrae is recommended as type and location of fracture can affect treatment and prognosis. Injury to the temporohyoid apparatus can lead to the fracture of portions of this apparatus, including petrous temporal bone fracture, and result in vestibular disease, cranial nerve disease, and occasional brain stem or hindbrain disease. Central nervous system (CNS) trauma accounts for 22% to 24% of neurologic disorders seen in equine hospitals, with spinal cord injury (SCI) being the most common. Studies investigating fatalities associated with high-speed equestrian sports found skull and axial spine fractures in 5% to 10% of fatalities. Listen to this lecture and more by Dr. Steve Reed starting at 12:30pm on Thursday, July 31st. 66

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