What is Big-Head Disease?

The typical swollen face and big head associated with nutritional secondary hyperparathyroidism.

Photo: Courtesy Dr. Rubén Anguiano

By Rubén Anguiano, MVZ, MSc, WEVA Regional Ambassador—México and Central America
Universidad de Guadalajara and Los Alamitos Equine Hospital, Guadalajara, México


Nutritional secondary hyperparathyroidism (NSHPT) is an uncommon endocrine pathology also known as “bran disease, Miller disease, big-head disease, osteitis fibrosa, swollen face disease, and equine osteoporosis.”

Horses that consume a diet low in calcium and/or high in phosphorus (typically with a phosphorus-to-calcium ratio of 3:1 or higher) can develop NSHPT. Horses that ingest grasses and toxic plants containing high concentrations of oxalate compounds, which inhibit calcium absorption, can be predisposed to developing NSHPT.

Excessive dietary phosphorus and decreased calcium absorption can lead to hypocalcemia (a low blood calcium concentration), hyperphosphatemia (elevated blood phosphorus levels), and hyperparathyroidism (hyperactivity of one or more parathyroid glands) in horses. Hyperphosphatemia stimulates parathyroid hormone (PHT) secretion and inhibits renal 1,25[OH]2D (quite simply, a form of vitamin D) synthesis. Low 1,25(OH)D2 concentrations contribute to parathyroid cell hyperplasia (increased cell growth) and PTH hypersecretion. Parathyroid hormone increases osteoclastic (breaking down bone) activity and results in excessive bone resorption and loss. Facial bone loss and excessive accumulation of unmineralized bone matrix (called osteodystrophy fibrosa) results in facial enlargement.

Poor body condition resulting from big-head disease.

Photo: Courtesy Dr. Rubén Anguiano

Because this a slowly progressive condition, homeostatic mechanisms (which contribute to homeostasis, enabling the body to function at an optimum steady state) could actually help maintain calcium levels close to or within the normal range.

Clinical signs include intermittent shifting lameness and a stiff gait, swollen facial bones, and mandibular (jaw) enlargement. Bone resorption around the molars and premolars can result in chewing problems, and teeth can become loose. Further, spontaneous vertebral fractures can occur, potentially resulting in posterior paralysis (partial paralysis of either or both hind limbs), and respiratory issues—such as nasal collapse, upper airway obstruction, and dyspnea (difficulty or labored breathing)—are common. Pregnant or lactating mares and young colts are most commonly affected; up to 15% of affected horses—typically those most severely affected—die.

Spontaneous fracture and posterior paralysis caused by nutritional secondary hyperparathyroidism.

Photo: Courtesy Dr. Rubén Anguiano

An important NSHPT outbreak recently occurred in in the state of Tabasco, México, and was related to complications from horses’ long-term ingestion of Pennisetum purpureum (more commonly known as giant, Napier, elephant, or Uganda grass), an oxalate-producing grass.

During that outbreak veterinarians diagnosed NSHPT using the horse’s history and clinical signs, radiographs, laboratory findings (including histopathology), and necropsy and examining the animal’s forage.

Treatment for affected horses included eliminating the oxalate source, adding alfalfa hay to the diet, and providing calcium carbonate and calcium phosphate supplementation. Horses in severe pain were confined and treated with non-steroidal anti-inflammatory drugs.

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