Bit & Bridle

Equine Myeloencephalopathy (EHM)

Other Names

  • Equine Herpes Myeloencephalitis (EHM)
  • EHV-1 Myeloencephalopathy
  • Neurological EHV-1
  • Equine Herpesvirus Neurological Disease

What is Equine Myeloencephalopathy (EHM)?

Equine Herpesvirus Myeloencephalopathy (EHM) is a neurological disease in horses caused by equine herpesvirus-1 (EHV-1). It represents the most serious and feared manifestation of EHV-1 infection and is characterised by inflammation and damage to the blood vessels supplying the brain and spinal cord, leading to ischaemic tissue injury (damage from restricted blood flow) and the progressive loss of neurological function.

EHM has gained significant prominence in recent years following a number of major outbreaks at equestrian events — most notably a severe outbreak at a cutting horse competition in Ogden, Utah in 2011, and several significant outbreaks in Europe and Australia. These events highlighted the potential for EHV-1 to spread rapidly among horse populations that congregate at competitions and sales, and prompted widespread review of biosecurity protocols at equine events globally.

Importantly, EHM can occur without preceding respiratory illness — some horses develop neurological signs as the first indication that they are infected with EHV-1. This makes early identification challenging, as respiratory illness is the more familiar face of EHV-1 infection. The neurological form tends to affect older horses more severely, and prior vaccination does not reliably prevent EHM.

Causes

EHM occurs as a complication of EHV-1 infection in a subset of affected horses. The mechanism involves:

  • Primary EHV-1 infection or reactivation: The virus either infects the horse for the first time or — more commonly in adults — reactivates from a latent state within peripheral blood mononuclear cells (the cells in which EHV-1 establishes lifelong latency).
  • Viraemia and T-cell-associated dissemination: The virus spreads via infected mononuclear cells to endothelial cells (the cells lining blood vessels), including those supplying the brain and spinal cord.
  • Vasculitis and thrombosis: EHV-1 infection of endothelial cells triggers an inflammatory cascade (vasculitis) and promotes blood clot formation (thrombosis) within the small blood vessels of the central nervous system.
  • Ischaemic neural injury: Reduced or blocked blood flow to neural tissue causes ischaemia (oxygen deprivation), leading to cell death and loss of neurological function in the regions supplied.

The neuropathogenic potential of EHV-1 is strongly associated with a specific point mutation (aspartate to asparagine at position 752, D752N) in the viral DNA polymerase gene. Strains carrying this mutation are more likely to cause EHM, though neurological disease can occasionally occur with wild-type (non-D752) strains. PCR assays that differentiate between these strains are available and are used during outbreak investigations.

Risk factors for developing EHM include older age, immune compromise, stress (from transport or competition), and potentially prior vaccination status — though this remains controversial.

Symptoms and Signs

  • Fever: Often the first sign — a rectal temperature above 38.5°C (101.3°F). Fever may precede neurological signs by several days and may resolve by the time neurological signs appear, or two distinct fever peaks (biphasic) may be present.
  • Nasal discharge: Present in some but not all horses — respiratory signs may be mild or absent.
  • Hindlimb incoordination (ataxia): The hallmark neurological sign. The horse appears unsteady, particularly in the hindlimbs, with a wide-based stance and a tendency to sway or stumble. Affected horses may drag their hindlimbs.
  • Weakness: Hind or occasionally all-limb weakness, which may progress to an inability to bear weight.
  • Urinary incontinence and dribbling: Bladder dysfunction — the horse fails to urinate normally or dribbles urine continuously. This indicates involvement of the sacral spinal cord segments controlling bladder function.
  • Faecal retention or overflow incontinence: Loss of rectal tone and defaecation control.
  • Loss of tail tone.
  • Recumbency: Severely affected horses may be unable to stand. Horses that become recumbent carry a much poorer prognosis than those that remain standing throughout their illness.
  • Cranial nerve deficits: Some horses develop facial nerve paralysis, difficulty swallowing, or head tilt if brain stem areas are affected.

Diagnosis

  • PCR testing of nasal swabs and whole blood: Real-time PCR is the cornerstone of diagnosis. Testing both nasal swabs and EDTA blood samples (a buffy coat preparation enriched for mononuclear cells) maximises sensitivity. The D752 mutation assay can also be run to identify neuropathogenic strain involvement.
  • Serology: A single serum sample is insufficient for diagnosis; paired samples showing a fourfold rise in titre over 2–3 weeks support recent active infection. In an acute neurological outbreak, PCR is the preferred diagnostic tool.
  • Cerebrospinal fluid (CSF) analysis: CSF sampling via atlantooccipital or lumbosacral centesis may show xanthochromia (yellow discolouration indicating haemorrhage) and elevated protein, consistent with CNS vasculitis. EHV-1 PCR on CSF is less sensitive than nasal swab or blood PCR but may be positive in some cases.
  • Neurological examination: A systematic neurological assessment (gait, tail and anal tone, perineal sensation, cranial nerve function) defines the distribution and severity of deficits and provides a baseline for monitoring progression or improvement.
  • Exclusion of other causes: EPM (equine protozoal myeloencephalitis — prevalent in North America), equine grass sickness, cervical vertebral stenotic myelopathy (wobbler syndrome), and other neurological conditions must be considered in the differential diagnosis.

Treatment

  • Corticosteroids: Dexamethasone is used early in the disease course to suppress the inflammatory vasculitis that drives neural damage. Early administration (before or during the febrile phase) may prevent the development of severe neurological signs. However, corticosteroids are immunosuppressive, which must be weighed against the anti-inflammatory benefit.
  • Antiviral therapy: Valacyclovir (an oral prodrug of acyclovir) is commonly administered to reduce viral replication in acutely affected horses. It is most effective when started early. Ganciclovir (intravenous) may be used in severely affected horses. The evidence for clinical benefit is limited but the drugs are generally well tolerated.
  • NSAIDs: Flunixin meglumine (Banamine/Finadyne) or phenylbutazone for anti-inflammatory and analgesic effects.
  • Bladder management: Regular manual emptying of the bladder (intermittent catheterisation, 3–4 times daily) is essential in horses with urinary dysfunction to prevent urinary retention, bladder over-distension, and ascending urinary tract infections.
  • Intensive nursing care: Horses that are recumbent require deep, well-maintained bedding, regular turning (every 4–6 hours) to prevent pressure sores, assistance to rise, and physical support. This is labour-intensive and may require round-the-clock care.
  • Intravenous fluids: For horses unable to drink or in poor systemic condition.
  • Dimethyl sulphoxide (DMSO): Sometimes administered as an intravenous infusion for its proposed anti-inflammatory and oxygen radical scavenging properties, though the evidence base in EHM specifically is limited.
  • Isolation and biosecurity: Strict isolation of affected and in-contact horses, cessation of horse movement, and implementation of biosecurity protocols are essential to prevent further spread within the facility. All horses in an affected facility should have rectal temperature taken twice daily.

Prevention

  • Vaccinate all horses against EHV-1 every 6 months. While vaccines do not reliably prevent EHM, they reduce overall viral replication and shedding, and may reduce the severity of disease.
  • Implement strict quarantine (21 days) for all new arrivals and horses returning from travel, competition, or contact with other horses.
  • Monitor all horses on affected premises twice daily for fever — isolate any horse with a temperature above 38.5°C immediately.
  • Avoid nose-to-nose contact between horses at competitions, and use your own equipment at all times.
  • Minimise unnecessary travel and competition attendance during periods of known EHV outbreaks.
  • Report confirmed or suspected EHV-1 outbreaks to your veterinarian and to national surveillance bodies (in the UK, the BEVA and the Animal Health Trust maintain EHV surveillance and can advise on management of outbreaks).

Prognosis

Prognosis depends heavily on the severity of neurological deficits. Horses with mild to moderate ataxia that remain standing throughout their illness have a reasonable chance of recovery — reported recovery rates in mild to moderate cases range from 60–90%. Horses that become recumbent carry a much poorer prognosis, and many are euthanised on welfare grounds due to the difficulty of nursing care and the risk of secondary complications (aspiration pneumonia, pressure sores, muscle myopathy). Even horses that recover clinically may have subtle residual neurological deficits and may not return to their previous level of performance. Bladder dysfunction, if it resolves, may take several weeks to months to normalise.

When to Call the Vet

Contact your veterinarian immediately if any horse in your care develops an unexplained fever (above 38.5°C/101.3°F), particularly if other horses in the same facility are also febrile or if the horse has recently returned from travel or competition. If neurological signs develop — wobbling, difficulty urinating, tail weakness, or falling — this is an emergency. Do not move any horses off the premises until you have spoken with your vet. Early treatment significantly improves prognosis. For related reading, see our entry on Equine Rhinopneumonitis (EHV-1 and EHV-4) and equine neurological health.

Frequently Asked Questions

Can a vaccinated horse get EHM?

Yes. Current EHV-1 vaccines available in the UK are not labelled for protection against the neurological form (EHM), and vaccinated horses have developed the disease. This is one of the most important limitations of current EHV-1 vaccines. However, vaccination is still recommended — it reduces overall viral load during infection and may lessen disease severity. Horses with higher antibody levels from recent vaccination may have some degree of protection. Research into improved vaccines targeting neuropathogenic strains is ongoing.

How contagious is EHM between horses?

EHM itself is not directly “contagious” as a neurological syndrome — not every horse exposed to EHV-1 will develop neurological disease. However, EHV-1 (the virus responsible) is highly contagious via nasal secretions, fomites, and aerosolisation. In a naive or stressed population, the respiratory form of EHV-1 can spread very rapidly, and a proportion of those infected may then develop EHM. This is why strict biosecurity measures are applied to the whole facility during an EHV-1 outbreak, not just to horses showing neurological signs.

What is the difference between EHM and wobbler syndrome?

Both conditions cause hindlimb incoordination in horses, but they have very different causes and management. Wobbler syndrome (cervical vertebral stenotic myelopathy, CVSM) is caused by compression of the spinal cord due to abnormal cervical vertebrae, is typically slowly progressive, and affects young, large-breed horses disproportionately. EHM is acute in onset, often accompanied by fever, and may be associated with bladder and bowel dysfunction. Radiographs, myelography, or CT of the cervical spine can differentiate CVSM, while PCR testing identifies EHV-1 involvement in EHM.

If my horse recovers from EHM, can it be ridden again?

Many horses that recover from mild to moderate EHM return to ridden work, though this may take several months. The severity and completeness of neurological recovery determine the horse’s long-term athletic prospects. Horses with significant residual ataxia or proprioceptive deficits should not be ridden, as this poses a safety risk. Your veterinarian will assess the horse’s neurological status once the acute phase has resolved and advise on the appropriateness of returning to work.