Other Names
Eastern equine encephalomyelitis (EEE), Western equine encephalomyelitis (WEE), Venezuelan equine encephalomyelitis (VEE), sleeping sickness (horses), equine encephalitis.
What is Equine Encephalomyelitis?
Equine encephalomyelitis refers to a group of viral diseases that cause inflammation of the brain and spinal cord (encephalomyelitis) in horses. The most clinically significant forms are Eastern equine encephalomyelitis (EEE), Western equine encephalomyelitis (WEE), and Venezuelan equine encephalomyelitis (VEE), each caused by distinct but related alphaviruses transmitted by mosquitoes.
These diseases are primarily endemic to the Americas — EEE is found along the eastern seaboard and Gulf Coast of the USA, WEE in the western USA and Canada, and VEE in Central and South America. In the UK and Europe, these specific viruses do not circulate naturally, but they are of global veterinary significance and are reportable diseases in many countries. Horses imported from affected regions and horses competing internationally may be at risk, and there are periodic concerns about the potential for mosquito-borne arboviruses to spread as climate changes alter vector ranges.
All three viruses are zoonotic — they can infect humans as well as horses. EEE is particularly dangerous in humans, with mortality rates of 30–70% in clinical cases. This makes EEE a public health concern wherever it circulates.
What Causes Equine Encephalomyelitis?
EEE, WEE, and VEE are caused by alphaviruses in the family Togaviridae. They are transmitted by mosquito vectors — primarily Culiseta melanura (EEE), Culex tarsalis (WEE), and various Aedes and Culex species (VEE).
The transmission cycle involves:
- Wild birds (passerine birds particularly for EEE and WEE) serve as primary reservoir hosts — they carry the virus without becoming ill
- Mosquitoes feed on infected birds and become infected
- Infected mosquitoes then bite horses (and humans), transmitting the virus
- Horses and humans are “dead-end” hosts — they develop high enough viraemia to become ill but not to infect mosquitoes back (except for VEE, where horses can be amplifying hosts)
Outbreaks are seasonal in temperate regions, coinciding with peak mosquito activity in summer and early autumn. Areas with standing water, wetlands, and warm temperatures support the highest mosquito vector populations and carry the greatest risk.
Symptoms and Signs
After infection, the virus crosses the blood-brain barrier and causes direct neuronal damage and inflammation of the brain and spinal cord. The incubation period is typically 5–15 days.
Early signs:
- Fever (often biphasic — a spike, brief improvement, then second fever as CNS invasion begins)
- Loss of appetite and depression
- Sensitivity to touch and sound (hyperaesthesia)
Progressive neurological signs:
- Altered mental state — dullness, lethargy, or in contrast, periods of excitement and agitation
- Head pressing against walls or objects
- Circling and impaired coordination (ataxia)
- “Sleeper” behaviour — the horse’s head droops, it appears to fall asleep standing (this gave rise to the common name “sleeping sickness”)
- Cranial nerve deficits — difficulty chewing, swallowing, facial asymmetry, abnormal eye movements
- Convulsions in severe cases
- Progressive inability to stand; recumbency indicates very poor prognosis
EEE tends to be more rapidly progressive and severe than WEE. Horses may progress from first signs to recumbency within 24–48 hours with EEE.
Diagnosis
Diagnosis requires laboratory confirmation in most cases, as neurological signs are not specific to encephalomyelitis. Differentials include rabies, West Nile virus disease, equine herpesvirus myeloencephalopathy, EPM, and hepatic encephalopathy.
Serology: Detection of IgM antibodies (indicating recent infection) by ELISA is the most practical ante-mortem test. Paired sera showing a significant rise in antibody titres can confirm recent infection. IgM capture ELISA for EEE and WEE is available at specialist laboratories.
PCR: Virus detection in blood is most successful in the early viraemic phase (before CNS invasion) and may be negative by the time neurological signs appear.
CSF analysis: Cerebrospinal fluid tap may show inflammatory changes consistent with viral encephalomyelitis.
Post-mortem: Brain histopathology shows characteristic lesions including neuronal necrosis and perivascular cuffing (inflammatory cells around blood vessels).
In the UK, any horse showing neurological signs should be investigated promptly — see also our entry on equine West Nile virus, another mosquito-borne neurological disease.
Treatment
There is no specific antiviral treatment for equine encephalomyelitis. Management is entirely supportive and symptomatic:
- Nursing care in a safe, padded environment to prevent self-injury in horses with altered consciousness or seizures
- Anti-inflammatory treatment — corticosteroids (dexamethasone) or NSAIDs to reduce brain swelling
- Anti-convulsants (diazepam, phenobarbitone) for horses with seizures
- Fluid therapy and nutritional support — nasogastric tube feeding for horses unable to eat
- Anti-oedema therapy — mannitol infusions to reduce intracranial pressure
- Dimethyl sulfoxide (DMSO) infusions are used by some veterinarians for suspected cerebral oedema
Horses that become recumbent and unable to rise have a very poor prognosis and may require humane euthanasia on welfare grounds.
Prevention and Vaccination
Vaccination is the most effective preventive measure in regions where EEE and WEE circulate. Combination vaccines against EEE, WEE, and VEE are widely used in the Americas and should be administered before mosquito season with a booster if the season is prolonged. In the UK, vaccination against EEE/WEE is not routinely performed but may be recommended for horses travelling to endemic regions.
Vector control measures:
- Reduce mosquito breeding sites — eliminate standing water in water troughs, buckets, and poorly drained areas
- Use insect repellents on horses during peak mosquito activity (dawn and dusk)
- Stable horses during peak mosquito activity times
- Install fine-mesh screens on stable windows and doors
For UK horse owners, the primary mosquito-borne neurological risk is West Nile virus, as the West Nile mosquito vector is established in parts of Europe including the UK periphery.
When to Call the Vet
- Any horse showing neurological signs — head pressing, circling, falling, seizures, loss of balance — requires urgent veterinary assessment
- A horse that becomes suddenly dull, unresponsive, or “sleepy” and fails to respond normally to stimuli
- Any horse returning from travel to or through endemic regions (USA, Central/South America) that develops fever followed by neurological signs
- A horse with fever that develops abnormal behaviour or altered consciousness within days
Prognosis
The prognosis varies significantly by virus type and severity. EEE carries the worst prognosis — mortality in unvaccinated horses can exceed 75–90%, and survivors may have permanent neurological deficits. WEE has a better prognosis, with mortality around 20–50% and a higher proportion of survivors recovering fully. VEE mortality is lower again (up to 40% in severe outbreaks), but can cause significant morbidity. Horses vaccinated before exposure and horses treated aggressively at the very earliest signs of disease have better outcomes than unvaccinated horses or those in whom treatment is delayed.
Frequently Asked Questions
Can equine encephalomyelitis affect horses in the UK?
EEE, WEE, and VEE do not currently circulate naturally in the UK or mainland Europe. The primary risk is to horses travelling to or competing in affected regions — particularly North and South America. However, as climate change alters the range of mosquito vectors, the potential for arboviruses to establish in new areas increases. Any horse returning from endemic regions should be monitored carefully for neurological signs in the weeks following return.
Is equine encephalomyelitis contagious between horses?
No, the encephalomyelitis viruses (EEE, WEE) are not transmitted directly from horse to horse. Transmission requires a mosquito vector. The exception is VEE, where horses can develop high enough viraemia to serve as amplifying hosts and infect mosquitoes, which then bite other horses or humans — making VEE of particular concern during outbreaks.
Can I catch equine encephalomyelitis from an infected horse?
You cannot contract EEE or WEE from direct contact with an infected horse, as these viruses require a mosquito vector for transmission. However, if you are in the same environment as an infected horse, the mosquitoes that infected the horse may also bite you. EEE is particularly dangerous to humans — always use insect repellent and protective clothing in areas where the disease is active.
How is equine encephalomyelitis different from West Nile virus?
Both EEE/WEE and West Nile virus cause neurological disease in horses and are transmitted by mosquitoes. They are caused by different virus families — alphaviruses (EEE/WEE) versus flavivirus (West Nile virus) — and their geographic distributions differ, though West Nile virus has spread much more widely globally. West Nile virus is now present in parts of Europe, making it of more immediate relevance to UK horse owners than EEE or WEE at present.