Nutritional Diseases of Horses
Reports of uncomplicated nutrient deficiencies in horses are rare. The nutrients most likely to be deficient are caloric sources, 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. The consequences of increased susceptibility to parasitism and bacterial infections may be superimposed over still other clinical signs. Simple excesses are more common. Nutrients most commonly given in excess of needs, leading to toxicity 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 the size of the gonads may be strikingly decreased, and estrus may be delayed. The immune system is adversely affected, resulting in increased risk of viral diseases. 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. The ability to perform work is impaired, and endogenous nitrogen losses increase as muscle proteins are metabolized for energy, causing muscle wasting.
Overfeeding high-calorie feeds results in obesity in horses and may contribute to developmental orthopedic disease in 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 maybe caused by either inadequate intake of high-quality protein 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 poor-quality hair and hoof growth, weight loss, and inappetence. In addition, there may be decreased formation of Hgb, RBCs, and plasma proteins. Milk production is decreased in lactating mares. The following liver enzymes have shown decreased activity: pyruvic oxidase, succinoxidase, succinic acid dehydrogenase, D-amino acid oxidase, DPN-cytochrome C reductase, and uricase. Corneal vascularization and lens degeneration have been noted. Antibody formation is also impaired.
Horses of all ages fed grass hay or pasture and supplemented with large amounts of 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. Serum alkaline phosphatase activity is usually increased, and clotting time may be prolonged slightly. Young, growing bone is frequently rachitic and brittle. Fractures may be common and heal poorly. Swelling and softening of the facial bones and alternating limb lameness are frequently reported. (Also see Osteomalacia.)
Phosphorus deficiency is most likely in horses 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. Sweat and urinary losses are appreciable. Horses deprived of salt tire easily, stop sweating, and exhibit muscle spasms if exercised strenuously. Hemoconcentration and acidosis may be expected. Anorexia and pica may be evident in chronic deprivation, although these are not specific signs of salt deficiency. In lactating mares, milk production seriously 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.
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. If body stores of vitamin A are high, signs may not appear for several months. The 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. Hooves are frequently deformed, with the horny layer unevenly laid down and unusually brittle. Metaplasia of the intestinal mucosa and achlorhydria have been reported. Genitourinary mucosal metaplasia may be expected. Bone remodeling is defective. The foramina do not enlarge properly during early growth, and skeletal deformities are evident. The latter may be seen in foals of vitamin A–deficient mares.
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 (see 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.
Although natural feeds plus synthesis within the gut normally provide adequate riboflavin, limited evidence indicates an occasional deficiency when the diet is of poor quality. The first sign of acute deficiency is catarrhal conjunctivitis in one or both eyes, accompanied by photophobia and lacrimation. The retina, lens, and ocular fluids may deteriorate gradually and result in impaired vision or blindness. Equine recurrent uveitis (see Equine Recurrent Uveitis) has been linked to riboflavin deficiency but may be a sequela of leptospirosis or onchocerciasis.
The normal feedstuffs of horses generally contain very little vitamin B12. However, horses can synthesize this vitamin in the gut, from which it is absorbed.