Equine Leukoencephalomalacia (ELEM) is a devastating neurological disease caused by ingestion of fumonisin mycotoxins produced by the fungus Fusarium moniliforme (and related species) that infect mouldy maize (corn). The toxins cause liquefactive necrosis of the white matter of the brain — a progressive destruction of the myelin-rich areas of the cerebral hemispheres that results in severe, often rapidly fatal neurological signs. ELEM is sometimes referred to as "mouldy corn poisoning" or "blind staggers" and has caused significant mortality in horse populations across the Americas, South Africa, and other maize-growing regions.
Other Names
- Mouldy corn disease
- Fusarium encephalitis
- Blind staggers (historical, though this term is also used for selenium toxicosis)
- Fumonisin toxicosis
What Is Equine Leukoencephalomalacia?
ELEM is a mycotoxicosis — a disease caused by fungal toxins rather than by a live infectious agent. The fumonisins (primarily Fumonisin B1 and B2) produced by Fusarium species disrupt sphingolipid metabolism at the cellular level, interfering with the synthesis of ceramide and sphingomyelin. Since myelin (the insulating sheath of nerve fibres in the brain's white matter) is rich in sphingolipids, it is particularly vulnerable. The result is focal liquefactive necrosis — areas of the brain literally liquefy, forming cavitated lesions that are visible on post-mortem examination.
The disease is not contagious. Horses become affected by eating feed containing sufficient concentrations of fumonisin-contaminated maize, and the disease can appear weeks to months after contaminated feed is introduced. Donkeys and mules are also susceptible. Pigs can develop pulmonary oedema from the same toxins (porcine pulmonary oedema), while poultry are relatively resistant.
Causes
ELEM is caused by the ingestion of fumonisins — mycotoxins produced when Fusarium moniliforme, F. proliferatum, and related species infect maize grain. The key conditions that favour fungal growth and toxin production include:
- Drought stress during maize growing season followed by insect damage to the grain
- Hot, humid conditions during storage
- Improper drying or storage of maize
- Visibly mouldy grain, cobs, or maize products
Fumonisin contamination is not always visible — grain may appear normal whilst harbouring dangerous levels of toxin. The threshold dose for ELEM in horses is not precisely established, but concentrations above 5–10 ppm in feed are considered potentially hazardous with prolonged exposure. Fumonisins are heat-stable and are not destroyed by pelleting, steam flaking, or cooking.
Risk factors include:
- Feeding maize-based diets, particularly whole corn, corn cobs, or homegrown maize
- Use of grain from drought-affected or insect-damaged crops
- Feeding mouldy or poorly stored grain
- Geographic location in maize-growing regions with hot, humid summers
Symptoms and Signs
ELEM has a variable onset — signs may appear within days of exposure to highly contaminated feed, or may only develop after weeks of lower-level continuous exposure. There are two overlapping clinical presentations: a primarily neurological form and a hepatic (liver) form, though the neurological form predominates in horses.
Neurological signs include:
- Apparent blindness — the horse walks into walls and cannot navigate familiar environments
- Head pressing against solid objects
- Ataxia and incoordination, often severe
- Circling or moving in one direction compulsively
- Apparent dementia — loss of recognition of familiar people and surroundings
- Dysphagia (difficulty swallowing)
- Profuse, uncontrolled sweating
- Seizures in severe cases
- Recumbency and inability to rise in terminal stages
Hepatic signs (more prominent in some cases) include:
- Jaundice (yellowing of mucous membranes)
- Depression and anorexia
- Elevated liver enzymes on blood work
Once neurological signs are severe, the disease progresses rapidly to death, typically within 1–3 days. Multiple horses in the same yard may be affected simultaneously if all are being fed from the same contaminated batch.
Diagnosis
A presumptive diagnosis can be made based on neurological signs, history of maize feeding, and the involvement of multiple animals. Definitive confirmation requires:
- Feed analysis: Submit samples from suspect feed batches for fumonisin testing — this is the most practical diagnostic step in a live outbreak
- Post-mortem examination: Gross pathology reveals characteristic cavitated, fluid-filled lesions in the white matter of the cerebral hemispheres. Histopathology confirms liquefactive necrosis.
- Blood biochemistry: May show elevated liver enzymes (AST, GGT, SDH), elevated bilirubin, and electrolyte disturbances, though these are non-specific
- Serum sphingoid base ratio: Elevated free sphinganine/sphingosine ratio in blood is a specific biomarker of fumonisin exposure, used in research settings
Treatment
There is no specific antidote for fumonisin toxicosis. Once clinical neurological signs are present, the prognosis is extremely poor and many horses die or require euthanasia despite intensive support. Management focuses on:
- Immediate removal of the suspect feed: This is the single most important intervention — all horses on the same feed must be moved to a clean, fumonisin-free diet immediately
- Supportive care: IV fluids, NSAIDs for comfort, nutritional support
- Anti-seizure medication: Diazepam or other anticonvulsants if seizures are present
- Dimethyl sulphoxide (DMSO): Used empirically as an antioxidant and anti-inflammatory agent for CNS injury, though evidence for efficacy in ELEM is limited
- Protective nursing: Horses with severe ataxia and blindness require a padded environment and careful monitoring to prevent self-injury
Horses with mild hepatic involvement and early-stage neurological signs may recover if feed is removed promptly, but those with moderate to severe neurological deficits rarely survive to a functional outcome.
Prevention
Prevention is entirely achievable through feed management:
- Source maize and maize-containing feeds from reputable suppliers with mycotoxin testing programmes
- Never feed visibly mouldy grain or hay to horses
- Store grain in cool, dry conditions with good ventilation — avoid damp storage
- Use grain within a reasonable period after purchase — do not stockpile large quantities in humid conditions
- Consider routine mycotoxin analysis of home-grown maize crops, particularly following drought or significant insect pressure
- Use commercial mycotoxin binders (such as bentonite clay or specific commercial products) as a prophylactic measure in high-risk situations — consult your vet before use
In the UK, maize is less commonly fed directly to horses than in parts of the Americas or Africa, but maize-based commercial compound feeds and chaff products are widely used. Reputable UK feed manufacturers test raw materials for mycotoxins. If sourcing maize products independently or from small local producers, independent testing is advisable.
Prognosis
The prognosis for ELEM once neurological signs have developed is poor to grave. Fatality rates of 60–90% are reported in affected horses. Horses that survive the acute neurological phase may have residual cognitive deficits. Prevention and early feed removal in exposed but presymptomatic horses are far more effective than treatment.
When to Call the Vet
This is an emergency. Call your vet immediately if:
- Any horse shows sudden blindness, incoordination, head pressing, or disorientation
- Multiple horses in the yard are showing neurological or depressive signs simultaneously
- You suspect mouldy or contaminated feed has been ingested
- A horse is seizing or unable to stand
Remove all suspect feed immediately and secure a sample for laboratory testing before disposal. For related conditions, see Equine Motor Neuron Disease (EMND), which also causes progressive neurological dysfunction, and Equine Night Blindness. Our horse terminology guide on the equine nervous system provides useful context for understanding these conditions.
Frequently Asked Questions
Can horses recover from ELEM?
Recovery is possible if the disease is caught very early — before significant brain necrosis has occurred. Horses with only mild signs and early hepatic involvement sometimes recover if feed is removed promptly and supportive care is given. However, once moderate to severe neurological signs are present, recovery is uncommon and those that do survive may have permanent deficits.
How much mouldy feed does it take to cause ELEM?
The dose required depends on the concentration of fumonisin in the feed and the duration of exposure. Prolonged feeding of feed containing even low levels (5–10 ppm) can cause disease over weeks. A single large dose of heavily contaminated feed can cause disease within days. Because fumonisin content varies even within a single batch of grain, predicting a safe threshold is difficult — the safest approach is to never feed any visibly mouldy feed.
Is ELEM a risk if I feed commercially produced horse feeds?
The risk is very low with reputable commercial feeds. Major equine feed manufacturers in the UK and Europe test raw materials for mycotoxin contamination as part of their quality assurance processes. The risk is higher when using home-grown maize, purchasing grain directly from agricultural sources without mycotoxin testing, or feeding grain that has been stored poorly.
What should I do if I suspect contaminated feed?
Remove all suspect feed immediately and keep all horses that may have been exposed under close observation. Retain a sample of the feed in a sealed bag for laboratory fumonisin analysis. Contact your vet immediately if any horse is showing neurological or hepatic signs. Notify other horse owners in your area who may have purchased feed from the same source.