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Equine Herpesvirus Myeloencephalopathy: The Neurological Form of a Common Horse Virus

EHM (Equine Herpesvirus) at a Glance

50–90%
Horses Exposed
2–10%
Develop Neuro Signs
$2,000–10K
Outbreak Cost
14–21 Days
Quarantine Peroid
EHM is the neurological form of EHV-1 infection. It can cause devastating outbreaks in barns with mortality rates of 30–50% in neurological cases.
Neuro Signs
Biosecurity
PCR Testing
Vaccinate
Quarantine
21-Day Hold

EHV-1 Clinical Outcomes

Fever Only 60% Respiratory Form 25% Abortion (mares) 5% Neuro (EHM) 10% Mortality (Neuro) 50%

Comparison

Feature EHV-1 Respiratory EHV-1 Neurologic (EHM) Key Difference
Signs Fever, cough, nasal discharge Ataxia, urine retention, recumbency Neuro signs = emergency
Onset 2–7 days post exp. 5–10 days post fever Often follows fever spike
Contagious Extremely (via nasal shed) Same virus strain Same transmission route
Treatment NSAIDs, rest, support Aggressive: antivirals, sling Requires hospital-level care

EHM Outbreak Response

Isolate Sick Test PCR Quarantine 21D Monitor Temp Biosecurity

EHM Biosecurity Checklist

Isolate any horse with fever of unknown origin
Take daily temperature of all barn horses
Test suspect cases with nasopharyngeal PCR
Quarantine exposed horses for 21 days minimum
Use dedicated equipment for each horse group
Disinfect stalls with accelerated hydrogen peroxide
Limit barn visitors during outbreak
Vaccinate stable against EHV-1? (ask vet about risk)
⚠️ EHV-1 is endemic — most horses are latently infected and can reactivate under stress. An outbreak can start from a single horse at a show.
✅ Vaccination reduces respiratory disease but does NOT prevent the neurological form. Biosecurity is the only reliable protection against EHM.

Equine herpesvirus myeloencephalopathy (EHM) is a neurological syndrome caused by equine herpesvirus type 1 (EHV-1) that affects the spinal cord and brain vasculature, causing ataxia, hindlimb weakness, bladder dysfunction, and in severe cases recumbency and death. Unlike EHV-1 respiratory or abortion strains, the neuropathogenic strain (distinguished by an N752 mutation in the DNA polymerase gene) causes vasculitis and thrombosis in CNS blood vessels rather than just upper respiratory infection. EHM occurs sporadically but can affect multiple horses at a facility simultaneously, making it a significant biosecurity concern.

EHM Phase Post-Exposure Timing Key Signs
Respiratory onset Days 3–7 Fever 102–106°F, nasal discharge, reduced appetite
Neurological onset Days 6–10 Second fever spike; symmetric hindlimb ataxia; bladder atony
Critical / recumbent Days 7–14+ Cannot rise; poor prognosis — intensive referral care required immediately
N752 mutation
Neuropathogenic EHV-1 strain marker — PCR differentiates it from standard respiratory strains
21-day quarantine
AAEP minimum from last fever case — no horse enters or exits during active quarantine period
Symmetric ataxia
Bilateral hindlimb pattern distinguishes EHM from trauma or wobbler — non-painful on palpation

How EHV-1 Becomes Neurological

EHV-1 is endemic in horse populations worldwide; most adult horses have been exposed. The virus establishes latency in trigeminal ganglia and lymph nodes, reactivating under stress (shipping, competition, illness, weaning). In most reactivations, horses shed virus nasally for 7 to 10 days and recover without neurological signs. In a subset of horses -- more commonly those exposed to the N752 neuropathogenic strain -- the virus infects endothelial cells of CNS vasculature, triggering inflammation, platelet aggregation, and ischemic infarcts in the spinal cord and brainstem.

Clinical Signs and Timeline

Initial signs are identical to standard EHV-1 respiratory infection: fever (102 to 106 degrees F), nasal discharge, and reduced appetite appearing 3 to 7 days after exposure. Neurological signs develop 6 to 10 days post-exposure as a second fever spike: symmetric ataxia beginning in the hindlimbs (like "walking on ice"), hindlimb weakness, urine dribbling from bladder atony, tail weakness, and reduced perineal sensation. Severely affected horses become recumbent within 24 to 48 hours of neurological onset; recumbent horses have a guarded to poor prognosis.

A key clinical marker: EHM typically affects hindlimbs symmetrically and is non-painful, distinguishing it from cervical spinal cord compression (wobbler syndrome) or trauma, which are often asymmetric or painful on palpation.

Diagnosis

Presumptive diagnosis is based on clinical signs plus PCR confirmation of EHV-1 in nasal swabs or whole blood. PCR can differentiate the neuropathogenic N752 strain from standard EHV-1 strains. Cerebrospinal fluid analysis shows xanthochromia (yellow-tinged CSF from hemoglobin breakdown) with elevated protein and minimal cell increase -- a characteristic pattern. Paired serum neutralization titers showing a 4-fold rise confirm active infection retrospectively.

Treatment and Biosecurity

No antiviral therapy has FDA approval for EHV-1 in horses. Valacyclovir (27 to 40 mg/kg orally every 8 hours for 7 days, then tapered) has demonstrated antiviral activity in pharmacokinetic studies and is used off-label at many referral hospitals. Supportive care includes IV fluids, NSAIDs (flunixin meglumine 1.1 mg/kg IV every 12 hours), bladder catheterization for atonic bladders, and deep bedding for recumbent horses with sling support.

Biosecurity is critical. Affected horses shed EHV-1 nasally and should be immediately isolated in a separate airspace (not just a different stall). Any horse with fever on the same premises should be quarantined. USDA and AAEP recommend a minimum 21-day isolation from the last fever case before ending a facility quarantine. No currently available EHV-1 vaccine reliably prevents EHM; modified-live EHV vaccines are contraindicated in outbreak settings.

Sources: American Association of Equine Practitioners (AAEP) EHV-1 Outbreak Management Guidelines (2012); Pusterla N et al., "Equine herpesvirus-1 myeloencephalopathy," Veterinary Journal (2009); USDA APHIS Equine Herpesvirus guidelines.

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