Nutritional Diseases of Horses

1. Nutritional Diseases of Horses

2. Mineral Deficiencies and Excesses: • Phosphorus Deficiency: • 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.

3. Salt Deficiency: • 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. • Hemoconcentrationand acidosis may be expected.

4. 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.

5. Potassium: • 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.

6. Magnesium: • Foals fed a purified diet containing magnesium at 8 mg/kg (3.6 mg/lb) exhibited hypomagnesemia, nervousness, muscular tremors, and ataxiafollowed 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.

7. Iron: • 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.

8. Zinc: • 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.

9. Copper: • 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.

10. Selenium: • Selenium deficiency results in reduced serum selenium, increased AST activity, white muscle disease, and perhaps rhabdomyolysis in working 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.

11. Vitamins: • 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.

12. Hooves are frequently deformed • 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.

13. 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..