Discussion

Equine herpesvirus-1 (EHV-1) is, for multiple reasons, a problematic infectious disease in the horse. EHV-1 may cause several different clinical syndromes, some of which result in epidemics of disease following the arrival of an infected horse on the premises. The virus can also be maintained in carrier animals, which may then result in either self-disease (most likely) and/or spread at some later point in time. Recent studies have shown that carrier horses given very large and repeated doses of dexamethasone will have viral reactivation at only low levels and no or limited transfer of the virus to in contact horses. This helps explain why we have rarely had EHV-1 outbreaks or spread in hospital housing although stressed or corticosteroid treated horses are commonplace and undoubtedly some are carriers. Spread of the virus is mostly horse to horse as its persistence in the environment is relatively short. Transmission is typically via infected nasal secretions, although fetal membranes and placental fluid from the aborted fetus are also highly infective. After direct contact, the virus first colonises the nasal mucosa and then replicates in regional lymph nodes by 1 - 3 days. This is followed by viraemia for 3 - 14 days (depending upon the strain). From Day 2 or 3 post infection to at least Day 7, there should be high virus load in nasal secretions. With high virus loads and the appropriate host (mostly older horses with low levels of cytotoxic T lymphocyte response to EHV1) there might be sufficient transmission of EHV-1 from lymphocytes to CNS endothelial cells to cause acute CNS disease.
Outbreaks of acute neurological disease are usually associated (83%) with a mutation in the polymerase gene, the mutant virus's suppression of chemokines and cytokines, and high levels of viraemia resulting in CNS vasculitis. Outbreaks of EHV-1 myelopathy are the rule with fever (biphasic), posterior ataxia and dysuria common findings. Oedema of limbs and nasal discharge may also be seen. On rare occasion an isolated neurological case occurs. Outbreaks seem to be most common at boarding stables, show facilities, broodmare farms. Horses clinically affected with acute EHM will be shedding virus and should be managed with strict biosecurity although they were likely shedding even greater amounts of virus during their initial fever which is generally 3 - 4 days before the onset of neurological signs. Treatment should include moderate to high doses of dexamethasone for severely affected or progressive cases, aspirin and/or clopidogrel, catheterisation of the bladder if dysuria is present, antibiotics if bladder catheterisation is needed and valacyclovir. Horses that become recumbent rarely return to athletic function. Chronic dysuria and incontinence can persist in some horses even after the gait appears to return to normal. There is no definitive proof to my knowledge to suggest that a superior vaccine is available!
Temporohyoid osteoarthropathy (THO) is a sporadic but not rare neurological disorder of adult horses. Since 2000, we have examined 24 horses with this condition. The aetiology of this arthritic disease is unknown. It is a degenerative arthritis that is in some cases associated with cribbing. The disease is most common in middle aged horses, the youngest being 3 years of age, and approximately 40% have bilateral disease, although the clinical signs are almost always unilateral. The signs are variable with some horses having behavioural signs associated with being ridden or while eating; these are likely signs of pain. Acute onset of neurological signs are believed to occur when the fused TH joint fractures. Fractures may be associated with sudden movements of the head and have been reported in horses being tubed or after dental procedures. Clinical signs are those associated with cranial nerve VII and/or VIII dysfunction. Diagnosis is by clinical signs, endoscopy of the guttural pouch, radiographs or computed tomography. Cerebrospinal fluid (CSF) is inflammatory in approximately 25% of cases and in a rare case, septic (consider Staph. aureus). Treatment goals are directed towards decreasing inflammation and infection, if present, and preventing complications, of which exposure keratitis is perhaps the greatest. Approximately 50% of the horses return to athletic use. We have routinely recommended a ceratohyoidectomy for both patient comfort and to prevent further fractures at the fused TH joint(s).
Trauma to the CNS continues to be a major cause of morbidity and mortality in horses. Horses experiencing acute brain trauma with either recumbency of several hours or those with fractures involving the basilar bones were associated with a poor prognosis. Specialised imaging may be helpful in these cases and in horses with other brain disorders. Horses with abnormal mentation due to brain disease are likely to have abnormal CT findings. For horses with cranial nerve deficits, the odds of finding a lesion on CT are lower. Treatments to decrease intracranial pressure, decrease inflammation, maintain perfusion and prevent infection are standard of care.
Recently, we have described a syndrome of symmetrical tetraparesis and ataxia and cervical pain associated with epidural haematoma (no known trauma) at C5 - C7. The onset is acute and severity of signs is often 3 - 4/5 ataxia.
Both equine motor neuron disease and equine degenerative myelopathy are associated with Vitamin E deficiency with EMND having a more causative link. Only EMND has an acute onset of clinical signs.
Neuroborreliosis has been documented in the horse with ataxia, muscle atrophy and nerve root signs (cervical or thoracolumbar) being the most common clinical signs. A marked CSF lymphocytic pleocytosis is usually present and upon necropsy, a marked lymphocytic (mixed size and type) meningitis with thickened dura and nerve root involvement has been found. There is a high CSF:Serum Borrelia antibody ratio suggestive of intrathecal production of Borrelia antibodies and PCR may be positive. Affected horses have responded favourably to tetracycline, doxycycline or minocycline treatments although relapses have occurred.
Botulism seems to have an increase in incidence associated with the feeding of 'round bales' in the US. Equine protozoal myelitis continues to be a problematic disease in North America. Parelaphostrongylus tenuis infection can cause an acute in young horses.