Big Head Disease (Oxalate Toxicosis) in Horses

Key Takeaways

Oxalate toxicosis occurs when horses ingest a toxic dose of oxalates, which are naturally occurring acid compounds that can be found in a number of plant species. Once ingested, the oxalate acids bind to calcium in food sources, preventing absorption of calcium by the body. 

• In its chronic form, also referred to as “big head” disease, oxalate poisoning causes demineralization of bone and abnormal bony swelling of the head

• Common symptoms of oxalate toxicosis include muscle tremors, lethargy, weight loss, colic, and frequent bone fractures

• Diagnosis is based on history of exposure, blood tests, and physical examination

• Treatment options include IV calcium,  calcium supplements and supportive care

• Due to the limited amount of treatment options and the absence of an antidote, prevention is crucial in ensuring the animal’s well-being

A Closer Look: What is Oxalate Toxicosis in Horses?

Non-ruminant animals such as horses are highly susceptible to excessive oxalate levels, as they are not able to degrade oxalate in their diet into non-toxic compounds. 

Oxalate-containing plants include:

• Halogeton (Halogeton)

Setaria grass 

• Lambsquarter (Chenopodium)

• Purslane (Portaluca)

• Kikuyu grass (Cenchrus)

Brassica species

• Redroot pigweed (Amaranthus)

• Common mallow (Malva)

• Dock (Rumex)

• Soft roly poly (Salsola)

• New Zealand spinach (Tetragonia)

Oxalate toxicosis can be characterized as acute or chronic. 

Acute oxalate toxicosis occurs when large amounts of oxalate acids are ingested over a short period of time. The resulting sudden decrease in calcium levels causes: 

Muscle tremors • Lethargy • Weakness • Colic

• Collapse • Seizures • Loss of consciousness

Chronic oxalate toxicosis: also referred to as nutritional hyperparathyroidism or “big head” disease, is caused by the ingestion of oxalate-containing plants over the course of months. The ingestion of oxalates leads to calcium deficiency, causing weakening of the bones. Symptoms of secondary nutritional hyperparathyroidism include:

Decreased appetite 

• Weight loss 

• Bone fractures

• Enlarged head

• Shifting weight when standing

Lameness, particularly lameness that tends to change limbs

• Increased urination

• Increased thirst

There is no antidote or specific treatment available; as such, prevention is the best way to ensure the animal’s health.

Risk Factors

Oxalate toxicosis is uncommon in horses. This toxicosis can cause severe calcium deficiency. Left untreated, it can cause life-threatening kidney failure. Horses with symptoms of oxalate toxicity require prompt veterinary care.

Horses under the age of three, lactating mares, performance horses, and those with immune disorders are at greater risk of oxalate toxicosis, due to high dietary calcium demands. Foals are at particular risk as calcium imbalances at an early age can cause improper skeletal development.

Possible Causes

The specific mechanism of oxalate toxicosis is complex and involves a number of factors. Once ingested, oxalates bind to calcium and magnesium sources, preventing proper absorption of these minerals. The reduction of calcium intake causes bone demineralization.

Main Symptoms

Common symptoms of oxalate toxicosis include: 

Muscle tremors • Lethargy • Difficulty breathing 

• Recumbency • Weakness • Seizures

Abdominal pain (colic)

Testing and Diagnosis

Horses presenting with symptoms of oxalate toxicosis generally undergo the following diagnostics: 

• Physical examination 

• Diagnostic imaging, including X-rays of the head

• Feed analysis 

• Bloodwork

Steps to Recovery

The first step in treatment is removing the oxalate source. 

There is no antidote for oxalate toxicosis, as such treatment is of a supportive and symptomatic nature. Treatment options include: 

• IV calcium

• Calcium supplements 

• Fluid therapy and electrolytes

Repeated bloodwork is required to monitor progress and ensure that no electrolyte imbalances arise from calcium supplementation. 

Prognosis of oxalate toxicosis varies greatly and depends on the amount of toxin ingested, the severity of bone damage, and the timing of treatment. Horses that survive an acute toxicosis often develop kidney failure, and have a poor prognosis. Horses with chronic toxicosis may have kidney damage and long-term lameness issues relating to demineralization of bones. Growing horses suffer the most serious consequences of chronic toxicosis, as their growing bones are unable to mineralize properly which may lead to orthopedic problems later in life.


Oxalate toxicosis is not contagious. 

Horses that do not ingest oxalate-containing plants do not develop oxalate toxicosis. Strategies for prevention include:

• Inspecting fields and feed prior to grazing or feeding 

• Providing a healthy and balanced diet with appropriate calcium levels

• Providing an alternative forage source if horses are turned out in contaminated pastures

• Feeding alfalfa: alfalfa is high in calcium

Is Oxalate Toxicosis Common in Horses?

Oxalate toxicosis is uncommon in horses.

Typical Treatment

• IV calcium

• Calcium supplements 

• Fluid therapy

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