Equine herpesvirus myeloencephalopathy, or EHM, is a neurological disease in horses caused by equine herpesvirus type 1 (EHV-1). It occurs when the virus, which more commonly causes respiratory illness and abortion, spreads through the bloodstream and damages blood vessels in the brain and spinal cord. EHM can range from mild hind-limb wobbliness to complete paralysis, and in severe cases it is fatal. The condition has drawn increasing attention from veterinarians and the equine industry because outbreaks at large gatherings can spread fast and existing vaccines do not reliably prevent it.
How EHV-1 Turns Into a Neurological Disease
Most horses encounter EHV-1 at some point in their lives, usually through respiratory contact. In the typical scenario, the virus causes a fever, nasal discharge, and a cough that resolves within a couple of weeks. In a smaller fraction of infections, the virus hitches a ride on white blood cells circulating in the bloodstream and reaches the blood vessels of the central nervous system. Once there, it infects the cells lining those small vessels, triggering inflammation and damage known as vasculitis.1PubMed. Equine herpes myeloencephalopathy The resulting swelling and clotting cuts off blood flow to portions of the spinal cord and, less often, the brain. The neurological signs a horse develops depend on exactly where this blood supply gets interrupted.
The process is sometimes described as a kind of stroke within the spinal cord. Areas starved of oxygen undergo infarction, and surrounding tissue can show axonal degeneration, swollen myelin sheaths, and thick cuffs of immune cells around damaged vessels.2PubMed Central. Histopathologic Findings Following Experimental Equine Herpesvirus 1 Infection of Horses The immune system’s own aggressive response to the infection contributes to the tissue damage, which is why anti-inflammatory treatment is part of managing EHM cases.
The Genetic Mutation That Makes Some Strains More Dangerous
Not all EHV-1 strains are equally likely to cause neurological disease. A single change in the virus’s genetic code, specifically in the gene encoding its DNA polymerase enzyme, is strongly linked to neuropathogenic potential. Strains carrying one version of that gene (referred to as D752) are far more likely to cause EHM outbreaks than strains carrying the alternate version (N752).3PLOS Pathogens. A Point Mutation in a Herpesvirus Polymerase Determines Neuropathogenicity The neuropathogenic variant appears to replicate more efficiently in white blood cells, giving it a better ride through the bloodstream to the spinal cord.4The Journal of Infectious Diseases. A Single‐Nucleotide Polymorphism in a Herpesvirus DNA Polymerase Is Sufficient to Cause Lethal Neurological Disease
This genetic marker is useful for surveillance, but it is not destiny. In one large retrospective analysis covering over two decades of isolates, strains carrying the neuropathogenic variant were associated with dramatically higher odds of neurological disease. Yet about a quarter of confirmed EHM cases in that study involved viruses that carried the supposedly “non-neurologic” variant, meaning other host and viral factors clearly play a role too.5PubMed Central. Investigation of the prevalence of neurologic equine herpes virus type 1 (EHV-1) in a 23-year retrospective analysis (1984-2007) The horse’s own immune status, age, and stress level all influence whether an infection stays respiratory or progresses to EHM.
Recognizing the Signs
EHM typically begins with a fever, which can appear a few days after exposure to EHV-1. Some horses show respiratory signs first, such as a runny nose or mild cough, before neurological symptoms emerge. In other cases, especially in older horses, respiratory illness may be minimal or absent entirely, and the fever itself may be the only early warning sign.
Once the virus reaches the spinal cord vasculature, neurological signs develop over hours to a few days. The hallmark is hind-limb weakness and incoordination, often described by veterinarians as ataxia. A horse may sway while standing, drag its hind hooves, or have trouble backing up. Other common signs include:
- Bladder dysfunction: inability to urinate normally, sometimes requiring catheterization
- Loss of tail tone: the tail hangs limply and the horse cannot raise it
- Proprioceptive deficits: the horse seems unaware of where its hind limbs are positioned
- Recumbency: in severe cases, the horse goes down and cannot stand
A case report of a 17-year-old mare illustrates the typical presentation: she developed an acute fever, hind-limb weakness, and bladder dysfunction, with examination revealing ataxia and proprioceptive deficits concentrated in the hind end.6PubMed. Medical management and positive outcome after prolonged recumbency in a case of equine herpesvirus myeloencephalopathy Front-limb involvement does occur but is less common and usually less severe. In rare cases, EHM can affect the brainstem, producing head tilt, difficulty swallowing, or facial paralysis.
Who Is Most at Risk
Age is one of the clearest risk factors. Older horses are considerably more susceptible to developing EHM when infected with EHV-1. In experimental infections comparing yearlings with older mares, all young horses developed respiratory disease and a two-phase fever, but only one out of nine showed neurological signs. In contrast, every old mare developed EHM, and six of the nine had to be euthanized. Researchers have estimated that the incidence of EHM rises above 70% in female horses over 20 years of age. A California outbreak analysis found that each additional year of age increased the odds of becoming an EHM case by about a third.7PubMed Central. Identifying Host-Characteristics and Management Risk Factors in a California Equine Herpesvirus Myeloencephalopathy (EHM) Outbreak
Management factors matter as well. In the same California analysis, horses that shared a barn with infected animals had substantially elevated odds of developing EHV-1 infection or EHM, reflecting the highly contagious nature of the virus in close quarters.7PubMed Central. Identifying Host-Characteristics and Management Risk Factors in a California Equine Herpesvirus Myeloencephalopathy (EHM) Outbreak Stress from transportation, competition, and commingling with unfamiliar horses at events are all recognized triggers that can reactivate latent virus or increase susceptibility to new infection.
How EHM Is Diagnosed
Diagnosis starts with the clinical picture: a horse develops a fever, followed within days by hind-limb ataxia, especially if other horses in the same barn or event have been febrile. But clinical signs alone are not enough to confirm EHM, because other neurological conditions in horses, such as equine protozoal myeloencephalitis and cervical vertebral malformation, can look similar. Laboratory testing is essential.
The gold standard for confirming EHV-1 infection is quantitative PCR testing, which detects viral DNA. Samples can be taken from nasal swabs, blood, or both. In horses already showing neurological signs, nasal swabs detect the virus in the vast majority of cases: one review found a detection rate of about 94% in nasal secretions from horses with suspected EHM, compared with 70% from blood samples.8PubMed Central. Viremia and nasal shedding for the diagnosis of equine herpesvirus‐1 infection in domesticated horses In horses with only fever and respiratory signs but no neurological involvement, detection rates drop considerably, to around 15% from nasal secretions and 9% from blood, likely because the virus is present in smaller quantities or for a shorter window during milder infections.
PCR can also identify which genetic variant of EHV-1 is present, which helps veterinarians and state veterinarians gauge the outbreak’s potential severity. Cerebrospinal fluid analysis sometimes shows elevated protein levels consistent with vascular damage, though this finding is supportive rather than definitive on its own.
Treatment
There is no cure for EHM. Treatment focuses on limiting viral replication where possible, controlling inflammation, and keeping the horse alive and comfortable long enough for the damaged tissue to recover.
Antiviral Therapy
Valacyclovir, an antiviral drug more commonly known for treating herpes infections in people, has shown the most promise against EHV-1 in horses. In an experimental challenge study, horses that received valacyclovir shed less virus from the nose and had lower levels of virus in the blood compared with untreated controls. The severity of ataxia in treated horses was reduced, though valacyclovir did not prevent ataxia from developing entirely.9PubMed Central. Efficacy of the early administration of valacyclovir hydrochloride for the treatment of neuropathogenic equine herpesvirus type-1 infection in horses Timing matters: the drug appears most helpful when given early, ideally before neurological signs have set in. Once the spinal cord vasculature has already been damaged, an antiviral can stop additional viral replication but cannot undo the harm already done. The required doses are large, making treatment expensive, and the drug must be given orally multiple times per day to maintain effective blood levels.
Supportive and Anti-Inflammatory Care
Anti-inflammatory drugs, including corticosteroids and nonsteroidal anti-inflammatories like flunixin, are commonly used to reduce the inflammatory damage to blood vessels. Some veterinarians administer dimethyl sulfoxide (DMSO) intravenously as an anti-inflammatory and free-radical scavenger, though evidence for its effectiveness in EHM specifically is largely anecdotal.
For horses that lose bladder function, catheterization prevents dangerous urine buildup and secondary urinary tract infections. Horses that become recumbent need intensive nursing care: frequent repositioning to avoid pressure sores, sling support when possible to get them partially upright, and careful monitoring for complications like colic. The mare described earlier who presented with prolonged recumbency ultimately improved over 34 days and was discharged with only mild residual weakness, illustrating that even severe cases can sometimes recover with sustained supportive care.6PubMed. Medical management and positive outcome after prolonged recumbency in a case of equine herpesvirus myeloencephalopathy
Prognosis and Long-Term Recovery
Outcome depends heavily on how severe the neurological signs are at onset. Horses with mild ataxia, grade 1 or 2 on the standard 5-point scale, generally recover well and can return to previous activity levels. Those that arrive at the clinic with severe ataxia (grade 4 or 5) have a much grimmer picture. In one study of show-jumping horses affected by EHM, horses admitted with ataxia graded at 4 out of 5 or higher had a substantially increased fatality rate and only about a 10% chance of returning to their pre-outbreak performance level.10Journal of Veterinary Internal Medicine. Long-term performance of show-jumping horses and relationship with severity of ataxia and complications associated with myeloencephalopathy caused by equine herpes virus-1
Complications worsen the outlook. Urinary dysfunction and signs of widespread vasculitis (swelling in the limbs, skin changes) both predict poorer outcomes. None of the horses in that study who developed both vascular and urinary complications returned to their previous performance level.10Journal of Veterinary Internal Medicine. Long-term performance of show-jumping horses and relationship with severity of ataxia and complications associated with myeloencephalopathy caused by equine herpes virus-1 The variation between outbreaks can also be striking: in a comparison of two separate EHM events caused by the same viral strain, the 2021 outbreak saw urinary complications in 64% of affected horses, while the 2023 outbreak produced zero urinary complications, suggesting that host and environmental factors drive a great deal of the clinical variability.11Journal of Veterinary Internal Medicine. Comparison of clinical variables and outcome of 2 natural equine herpesvirus myeloencephalopathy outbreaks induced by equine herpesvirus-1 A2254/N752 strain in sport horses
Why Current Vaccines Fall Short
Several vaccines are commercially available for EHV-1, including killed (inactivated) and modified-live virus formulations. They do help reduce the severity of respiratory disease and can decrease nasal shedding of the virus.12PubMed. Control of EHV-1 viremia and nasal shedding by commercial vaccines The problem is that preventing EHM requires stopping the virus from reaching the bloodstream and the spinal cord, and no current vaccine reliably does that. Modified-live vaccines have performed better than inactivated ones in experimental challenge studies, producing near-undetectable nasal shedding in one trial.13PubMed. Comparison of the efficacy of inactivated combination and modified-live virus vaccines against challenge infection with neuropathogenic equine herpesvirus type 1 (EHV-1) But across the full body of research, a systematic review and meta-analysis of randomized challenge trials concluded that vaccination produces only a slight and statistically nonsignificant improvement in clinical and virological outcomes overall.14PubMed. Efficacy of vaccination against equine herpesvirus type 1 (EHV-1) infection: Systematic review and meta-analysis of randomised controlled challenge trials
Data from real-world outbreaks have muddied the picture further. During the large 2021 EHM outbreak in Valencia, Spain, vaccinated horses actually had higher rates of neurological disease and higher fatality rates than unvaccinated horses.15PubMed Central. Equine Infectious Disease Risk Factors and Long‐Term Outcomes in Horses After the 2021 Outbreak of Equine Herpesvirus 1 Myeloencephalopathy, Valencia, Spain This does not mean the vaccines caused the disease. The more likely explanation is confounding: older, more valuable competition horses are both more likely to be vaccinated and more biologically susceptible to EHM. But the finding underscores that vaccination alone should not be relied upon to prevent neurological disease. It remains one layer in a broader prevention strategy that hinges on biosecurity and outbreak management.
Latent Infection and the Carrier Problem
One of the most frustrating aspects of EHV-1 is its ability to go latent, hiding quietly inside the horse’s body for years or even the rest of its life. The virus tucks itself into lymphoid tissue and nerve ganglia, where it is invisible to the immune system and undetectable by routine screening. In a study of Thoroughbred broodmares submitted for necropsy in central Kentucky, latent EHV-1 DNA was found in over half of the animals tested. About 18% of those latently infected mares harbored the neuropathogenic variant of the virus.16PubMed. Prevalence of latent, neuropathogenic equine herpesvirus-1 in the Thoroughbred broodmare population of central Kentucky
In experimental studies, viral DNA has been detected in trigeminal ganglia, lymph nodes, and other tissues well after recovery from primary infection, with no evidence of active viral replication taking place.17PubMed Central. Viral Load and Cell Tropism During Early Latent Equid Herpesvirus 1 Infection Differ Over Time in Lymphoid and Neural Tissue Samples From Experimentally Infected Horses The virus is dormant but not gone. Stress, transport, corticosteroid treatment, or illness can trigger reactivation, at which point the horse can start shedding virus again from the nose without showing any obvious signs of illness. This silent shedding is a major reason EHM outbreaks seem to come out of nowhere: the source horse often looks perfectly healthy.
Biosecurity During an Outbreak
When EHM is confirmed or strongly suspected in a group of horses, rapid isolation and quarantine are essential. Sick horses should be separated immediately, and movement of all horses on the premises should stop. The experience at a veterinary teaching hospital that detected EHM among its hospitalized patients illustrates the approach: a voluntary quarantine was imposed, admissions were halted, and serial PCR testing of every horse on site was used to track the virus’s spread and eventually shorten the quarantine period once new cases stopped appearing.18Journal of Veterinary Internal Medicine. Detection and Management of an Outbreak of Equine Herpesvirus Type 1 Infection and Associated Neurological Disease in a Veterinary Teaching Hospital
Horses with EHM can shed virus from the nose for an extended period. An investigation of a Canadian outbreak found that nasal shedding continued for at least nine days from the onset of neurological signs, and a high proportion of horses were probably shedding at the time neurological disease first became apparent. The researchers recommended maintaining biosecurity measures for a minimum of nine days after the onset of clinical signs, and more prudently for at least two weeks. They also stressed that monitoring rectal temperatures across the entire group is one of the most valuable early-warning tools, because a fever spike often precedes neurological signs by a day or more and flags horses that need immediate isolation and testing.19Journal of Veterinary Internal Medicine. Nasal Shedding of Equine Herpesvirus-1 from Horses in an Outbreak of Equine Herpes Myeloencephalopathy in Western Canada
Personnel management matters as much as horse management during an outbreak. People can carry virus on their hands, clothing, and equipment. Dedicated boots, gloves, and coveralls for the isolation area, strict hand washing between horses, and disinfection of shared tools (twitches, stomach tubes, water buckets) are all standard recommendations.
Choosing the Right Disinfectant
EHV-1 is an enveloped virus, which generally makes it susceptible to disinfection, but the choice of product and conditions matter more than many barn managers realize. A study testing five commercial disinfectants found that quaternary ammonium compounds, which are among the most popular barn disinfectants, failed to inactivate EHV-1 when used at cold temperatures even with a ten-minute contact time. At room temperature they required more than a minute of contact. Chlorine-based disinfectants performed better, achieving inactivation with just 30 seconds of contact at room temperature and still working at temperatures as cold as minus ten degrees Celsius if given ten minutes.20PubMed Central. Efficacy of five commercial disinfectants and one anionic surfactant against equine herpesvirus type 1
The practical takeaway: in cold-weather months, when EHV-1 outbreaks tend to be most common, standard quaternary ammonium barn sprays may not do the job if surfaces are cold and contact time is short. Switching to a bleach-based solution or ensuring longer contact times can make a real difference. Organic matter like manure and mucus also reduces disinfectant effectiveness, so cleaning surfaces before applying disinfectant is more than a nicety.
How Outbreaks Differ Even With the Same Virus
One of the puzzling aspects of EHM is how different two outbreaks can look even when the same viral strain is responsible. Researchers compared two EHM events in sport horses, both caused by the same genetic variant of EHV-1. The median ataxia grade at admission was the same in both outbreaks, yet the rates of vasculitis and urinary complications were wildly different: 64% of horses in the first outbreak showed vascular complications, versus 20% in the second, and 64% had urinary dysfunction in the first compared with none in the second.11Journal of Veterinary Internal Medicine. Comparison of clinical variables and outcome of 2 natural equine herpesvirus myeloencephalopathy outbreaks induced by equine herpesvirus-1 A2254/N752 strain in sport horses
These differences likely reflect the interaction between host immune responses and the virus. The age distribution of the affected group, the timing of the horses’ last EHV-1 exposure or vaccination, ambient stress levels, and even the speed of veterinary intervention can all shift the clinical picture. For barn managers and event organizers, the lesson is that past experience with EHM at a facility does not predict how the next outbreak will play out. Each one demands a fresh, aggressive response.