Reports of uncomplicated nutrient deficiencies in horses are rare. The nutrients most likely to be deficient are caloric intake, protein, calcium, phosphorus, copper, sodium chloride, and selenium, depending on age and type of horse and geographic area. Signs of deficiency are frequently nonspecific, and diagnosis may be complicated by deficiencies of several nutrients simultaneously. Simple excesses are more common in some regions. Nutrients most commonly given in excess of needs, leading to toxicity, metabolic disorders, or induced deficits of other nutrients, are energy, phosphorus, iron, copper, selenium, and vitamin A.
Many nonspecific changes found in horses with caloric deficiency can result from inadequate intake, maldigestion, or malabsorption. Weight loss is the cardinal sign of inadequate energy intake. In partial or complete starvation, most internal organs exhibit some atrophy. The brain is least affected, but growth, reproduction, and performance ability are most affected. The immune system is also adversely affected. The young skeleton is extremely sensitive, and growth slows or may completely stop. A decrease in adipose tissue is an early and conspicuous sign and is seen not only in the subcutis but also in the mesentery; around the kidneys, uterus, and testes; and in the retroperitoneum. Low-fat content of long bone marrow is a good indicator of prolonged inanition.
Overfeeding high-calorie feeds results in obesity in adult horses and may contribute to developmental orthopedic disease in young, rapidly growing horses. However, some horses, especially those that are sedentary, can become obese on only good quality hay or pasture. Obesity increases the risk of laminitis (presumably associated with relative insulin resistance) and colic, due to strangulation of the small intestine by pedunculated mesenteric lipomas. Obese horses and ponies have reduced heat and exercise tolerance.
A deficiency of dietary protein may be caused by either inadequate intake or lack of a specific essential amino acid. The effects of deficiency are generally nonspecific, and many of the signs do not differ from the effects of partial or total caloric restriction. In general, the horse will have a poor quality haircoat and hoof growth, weight loss, and inappetence. Milk production is decreased in lactating mares, and rapidly growing foals will be stunted. Antibody formation is also reduced and will affect immunity.
Horses of all ages fed grass hay or pasture and supplemented with large amounts of unfortified, grain-based concentrates or wheat bran are most likely to develop relative or absolute calcium deficiencies leading to nutritional secondary hyperparathyroidism. Excess phosphorus intake (Ca:P ratio <1) causes the same clinical signs. Blood concentrations of calcium do not reflect intake because of homeostatic mechanisms, although blood inorganic phosphorus may be increased because of mobilization of bone mineral content. Swelling and softening of the facial bones and alternating limb lameness are frequently reported. Serum alkaline phosphatase activity is usually increased, and clotting time may be prolonged slightly. Fractures may be common, and wounds in general heal poorly. (Also see Osteomalacia in Animals.)
Phosphorus deficiency is most likely in horses, especially those with higher needs (growing, lactating, performing) being fed poor-quality grass hay or pasture without grain. Serum inorganic phosphorus concentrations may be decreased, and serum alkaline phosphatase activity increased. Occasionally, serum calcium levels may be increased. An insidious shifting lameness may be seen. Bone changes resemble those described for calcium deficiency. Affected horses may start to consume large quantities of soil or exhibit other manifestations of pica before other clinical signs are apparent.
Horses are most likely to develop signs of salt (NaCl) deficiency when worked hard in hot weather or fed salt-deficient rations. Horses deprived of salt tire easily, stop sweating, and exhibit muscle spasms if exercised strenuously. Anorexia and pica may be evident in chronic deprivation, although these are not specific signs of salt deficiency. In lactating mares, milk production declines. Polyuria and polydipsia secondary to renal medullary washout may be seen in prolonged deficits.
Chronic dietary deficiency of potassium results in a decreased rate of growth, anorexia, and perhaps hypokalemia. However, most forages contain more than sufficient potassium for the average horse. Acute deficits due to sweat losses are more likely and may cause muscle tremors, cardiac arrhythmias, and weakness. Excess potassium intake, especially if given as a bolus PO or IV, also will induce cardiac arrhythmias such as atrial fibrillation and possibly cardiac arrest.
Foals fed a purified diet containing magnesium at 8 mg/kg (3.6 mg/lb) exhibited hypomagnesemia, nervousness, muscular tremors, and ataxia followed by collapse, with increased respiratory rates, sweating, convulsive paddling, and death after a few weeks. However, most commonly used feeds contain magnesium well in excess of the 70–100 mg/kg dry ration currently recommended. Oversupplementation of this mineral is more likely. Although the effects of excessive magnesium intake in horses have not been determined, based on data from other species, it may cause clinical signs of calcium deficiency.
Iron deficiency may be secondary to parasitism or chronic blood loss and results in microcytic, hypochromic anemia. However, it is highly unlikely that even anemic horses are iron deficient. Iron excess interferes with copper metabolism and also causes microcytic, hypochromic anemia. Blood transferrin concentrations are the most reliable method to determine the iron status of a horse.
Zinc deficiency in foals causes reduced growth rate, anorexia, cutaneous lesions on the lower extremities, alopecia, decreased blood levels of zinc, and decreased serum alkaline phosphatase activity. Excesses (>1,000 ppm) were associated with developmental orthopedic disease in young horses. The effects of excesses or deficits of zinc have not been documented in adult horses.
An apparent relationship between low blood copper concentrations and uterine artery rupture in aged parturient mares suggests reduced copper absorption with age or reduced ability to mobilize copper stores. Dietary deficiency may cause aortic aneurysm, contracted tendons, and improper cartilage formation in growing foals. Excessive copper intake may interfere with selenium and/or iron metabolism.
Selenium deficiency results in reduced serum selenium, increased AST activity, white muscle disease, and perhaps rhabdomyolysis in working horses. (Also see Nutritional Myopathies in Horses.) Selenium excesses of as little as 5 ppm in the ration cause loss of mane and tail hairs and sloughing of the distal portion of the hoof.
A vitamin A deficiency may develop if dried, poor-quality roughage is fed for a prolonged period (more than 6 months). If body stores of vitamin A are high, signs may not appear for several months. Deficiency is characterized by nyctalopia, lacrimation, keratinization of the cornea, susceptibility to pneumonia, abscesses of the sublingual gland, incoordination, impaired reproduction, capricious appetite, and progressive weakness in adult horses. Hooves may be deformed, with the horny layer unevenly laid down and unusually brittle.
Vitamin A toxicity is associated with bone fragility, bone exostoses, skin lesions, and birth defects such as cleft palate and micro-ophthalmia (based on data from both horses and other species).
Vitamin E is very labile and quickly lost with storage in both hays and commercial feeds. It is an important antioxidant, and deficiency has been reported to be associated with an increased incidence of rhabdomyolysis, impaired immune function, reproductive failure, and ocular lesions. Some prolonged, aggressive antibiotic treatments, such as recommended for equine protozoal myelitis, have also been reported to induce vitamin E deficits. Fresh forages, however, are excellent sources of vitamin E, and horses with free access to good pasture rarely need supplementation.
If sun-cured hay is consumed or the horse is exposed to sunlight, it is doubtful a vitamin D deficiency will develop. Prolonged confinement of young horses offered only limited amounts of sun-cured hay may result in reduced bone calcification, stiff and swollen joints, stiffness of gait, irritability, and reduced serum calcium and phosphorus. Clinical signs are easily reversible with supplementation or exposure to sunlight.
Signs of experimental thiamine deficiency include anorexia, weight loss, incoordination, decreased blood thiamine, and increased blood pyruvate. At necropsy, the heart is dilated. Similar signs have been seen in bracken fern poisoning. Under normal circumstances, the natural diet plus synthesis by microorganisms in the gut probably meet the need for thiamine. However, needs may be increased by stress.