Big Head Disease (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.

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.

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

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.

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.

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

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

Oxalate toxicosis is uncommon in horses.

• IV calcium
• Calcium supplements
• Fluid therapy