Nutritional Diseases of Horses

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.

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.