• D₂, like D), produced in skin, are activated by liver and kidney
• Alpha-tocopherol, is most active form of vitamin E
• K₁, like K₂ and K₃ (synthetic form), is activated in liver • B₁ is activated in liver and kidrey
• B₆ is activated in the body
• All other B vitamins and vitamin C are present in their active form in plant source feeds Body storage A and D, 3 to 6-month supply in liver. E and K less than 1 to 3-week useable supply. Less than a few weeks, except B_12, for which many months to years supply is stored. Deficiency symptoms A = Decreased feed intake, increased respiratory and intestinal disease, slow growth, wt loss, poor fertility, dull hair, anemia, tearing, and night blindness.
D = Decreased feed intake and growth, enlarged bone growth plates, and bone demineralization
E = Muscle damage and/or inflammation of body fat, and impaired immunity
K = Decreased blood clotting and hemorrhage B vitamins = Decreased feed intake, unthriftiness, and poor growth or weight loss.
Biotin = Hoof wall crumbling & tender soles.
Folic Acid, B₆ and B₁₂ = Anemia but deficiencies not reported in horses.
C = Decreased wound healing and capillary fragility resulting in bleeding and scurvy, but a deficiency hasn’t been reported in horses Toxicosis symptoms A = Decreased feed intake and growth, dull hair, anemia, and increased bone size
D = Reduced feed intake, performance or growth, weight loss, recumbency, debilitation.
E = Doesn’t occur clinically.
K₁ & K₂ = not toxic; K₃ = acute renal failure, depression, colic, bloody urine Toxicosis from ingestion of vitamins B and C doesn’t occur or is rare as excesses are readily excreted. Clinical usage Beta-carotene = Improve reproductive efficiency in mares not getting green forage—may help
A = Prevent deficiency in horses not on green forage.
D = Skeletal diseases and horses not getting sun or sun-cured feed—rarely indicated
E = Exertion-induced muscle damage, a deficiency, and to enhance immunity or reproduction—may help reproduction when not on green forage
K = Deficiency due to spoiled sweetclover, warfarin, oral antibacterials, or impaired fat absorption resulting in slow blood clotting. Nobenefit for bleeders (exertion-induced pulmonary hemorrhage). B₁ = Increase appetite and decrease tying-up and anxiety—of questionable benefit.
B_2, niacin & pantothenic acid = Rarely used.
B₆ = Anemia — rarely beneficial.
Biotin = Improve hoofs—helps some cases
Folacin = Ensure optimal performance of stabled horses during racing & training—questionable benefit
B₁₂ = Anemia, enhance performance and increase appetite—doubtful benefit
Choline = Fatty liver and heaves—questionable benefit
C = Bleeders and muscle damage, and enhance performance, fertility, and skeletal development—questionable benefit for all of these uses

For each vitamin, the minimum amount necessary for optimum health and performance, as well as the upper safe levels for prolonged continuous consumption, as compared to the amount generally present in common horse feeds, are given in Appendix Table 3. The amounts recommended are, for many vitamins, more than the amount needed to prevent clinical signs of a deficiency yet considerably less than that which produces toxicosis. As indicated in this table, unless growing forage constitutes a majority of the horse’s diet, adding additional vitamins A and E to the horse’s diet may be beneficial, although rarely is this necessary to prevent a clinically apparent deficiency.

The majority of commercial grain mixes for the horse contain vitamins added at a level high enough to meet or exceed optimum levels of vitamin intake when the amount of grain mix recommended is fed. However, the amount of grain mix recommended may be more than you want to feed because it may unnecessarily increase feeding costs, or because it may provide more dietary energy than needed. Situations in which vitamin supplementation may be needed or beneficial are:

TABLE 3–2 Vitamin Deficiencies and Excesses: Causes and Effects^a

^a The absence of a description of a vitamin deficiency or excess indicates that such a vitamin imbalance is not known to occur in the horse. Abbreviations: bw = body weight; DM = dry matter; ↑ = increase; ↓ = decrease; < = less than; > = greater than; HR = heart rate; IM = intramuscular; IV = intravenous.

In both situations 2 and 3, giving vitamins A and E may be beneficial. The amount given should be sufficient to supply the horse’s requirements as given in Appendix Table 3. Although this can be accomplished for vitamin A by giving an injection every 2 to 4 months, there is little body storage of vitamin E, and therefore it is best to feed it daily.

Vitamin activity is decreased by external factors such as sunlight, feed grinding, heat, and exposure to air, and by a number of internal factors that occur particularly in vitamin supplements. Losses during storage are greatest for vitamins A, D, K. and B₁ (thiamin) Table 3-3. However, since vitamin A is the only one of these vitamins that the horse obtains only from the diet, it is the only one whose loss during storage is generally a problem. The factor that has the greatest effect on the loss of vitamin A activity during storage is moisture. For example, after 3 months of storage, vitamin A retention in a feed was 88% when both temperature and moisture were low, 86% when only temperature was high, but only 2% when both were high. Vitamin activity is also lost during feed processing (Table 3-4).

Additional situations in which vitamin supplementation may be beneficial are:

TABLE 3–3 Vitamin Stability in Feeds

TABLE 3–4 Vitamin Stability During Feed Pelleting and Extrusion

^a At 140 to 220°F (60 to 105°C) for pelleting, and 230 to 350°F (110 to 175°Q for extrusion, for 0.5 to 3 minutes. Retention is highest the lower the temperature and conditioning time.

In all of these situations, a balanced supplement providing additional quantities of all vitamins, without excessive amounts of any specific vitamin, as given in Table 3-5, is best.

Many of the vitamins, when added to a feed that is not for immediate consumption, must be protected to maintain their activity and efficacy. Commercial vitamin suppliers accomplish this by coating the vitamins with things like gelatin, wax, ethylcellulose, or sugar. Many vitamins in an unprotected form are incompatible with other vitamins and minerals. For example, B₁ is incompatible with B₂, both are incompatible with B₁₂ in the presence of light, and most vitamins are prone to oxidative destruction by iron, copper, sulfates, sulfides, phosphates, and carbonates. It is difficult to prevent these destructive interactions in liquid vitamin preparations such as liquid hematinics, or “blood builders or tonics,” that contain iron, copper, or incompatible vitamins. Convincing evidence of biological activity of the vitamins in these products should be provided by the company selling them; if not, they are not recommended.

VITAMIN A

Utilization and Functions

Horses derive their vitamin A naturally and entirely from dietary carotenoid pigments present in plants, the major pigment being beta-carotene. Beta-carotene in the wall of the small intestine is cleaved by intestinal enzymes, with varying degrees of efficiency by different species, to yield two moles of vitamin A per mole of beta-carotene. Rats and chicks do this most efficiently, horses relatively inefficiently, and cats and mink not at all, deriving 1667, 400, and 0 IU of vitamin A activity per milligram of beta-carotene, respectively. One IU or USP unit of vitamin A is equal to 0.3 µg of retinol.

Until recently, it was believed that the only function of beta-carotene was as a source of vitamin A and, therefore, it could be replaced entirely by vitamin A. However, some of the beta-carotene that is not cleaved into its molecules of vitamin A is absorbed intact and transported to a number of body tissues and organs, including the fat, skin, and ovary for use and storage. Storage in the ovary is primarily in the corpus luteum. Absorbed beta-carotene and other carotene pigments in plants are responsible for the yellow coloration of fat, milk, skin, and egg yolks in animals and birds consuming feeds high in carotene, such as green grass. In the ovary, beta-carotene, rather than vitamin E or A, serves as an antioxidant and is used to assist in maintaining plasma vitamin A concentration. Beta-carotene in the corpus luteum is also involved in the control of progesterone secretion and, as a result, the control of ovulation, embryo implantation, and pregnancy maintenance. These activities are therefore impaired by inadequate amounts of beta-carotene and cannot be corrected by vitamin A.

TABLE 3–5 Vitamin Supplements for Horses^a

Upon absorption, vitamin A is transported to the liver for storage, rather than to the ovary for storage as is beta-carotene. Vitamin A is either released from the liver into the blood for transport to the tissue for use, or excreted in the bile; that which is not reabsorbed is excreted in the feces. Small amounts of the vitamin A and its metabolites may also be excreted in the urine.

In the retina, vitamin A metabolites combine with the protein opsin to form rhodopsin (known as visual purple), which is necessary for vision, particularly at night. Vitamin A is also needed for bone and muscle growth, reproduction, and maintenance of healthy skin. It is thought that its mode of action in these activities is as a participant in the synthesis of glycoproteins that control cell differentiation and gene expression. A deficiency or excess of vitamin A affects and manifests by alterations in these functions.

Vitamin A Sources

Since vitamin A is not produced in the body, except from its precursors, it or its precursors, primarily beta-carotene, must be consumed in the diet. The concentration of vitamin A precursors in the vegetative portions of plants varies widely. Most grains are almost devoid of them, the exception being yellow corn (maize), which has a small amount (2 to 4 mg/kg). Beta-carotene is present in its highest concentration in green forage leaves and yellow vegetables. Carotenes in growing pasture grass and alfalfa (lucerne) may reach 300 to 600 mg/kg of dry matter (equivalent to 120,000 to 240,000 IU of vitamin A for the horse/ kg), whereas carotenes in high-quality hay (U.S. No. 1) are 20 to 40 mg (8,000 to 16,000 IU) and in poor-quality hay (U.S. No. 3) are only 4 to 5 mg (1,600 to 2,000 IU)/kg of dry matter. This is compared to the 2,000 to 3,000 IU/kg recommended in the horse’s total diet dry matter recommended (Appendix Table 3). If cut forage is rained on and the period of field drying is extended, appreciable leaf loss may occur prior to storage and feeding, resulting in a serious decrease in the hay’s carotene as well as vitamin E, protein, and dietary energy content.

Regardless of the type of forage, hay or pasture, if it contains any significant amount of green color and constitutes the majority of the horse’s diet, it will provide an adequate amount of beta-carotene, and also alpha-tocoph-erol (vitamin E), for optimum benefit for the horse, and therefore, additional amounts of either vitamin are unlikely to be of any benefit. Although carotenes are a yellow-orange pigment, the amount of green color present in forage gives a rough approximation of the amount of beta-carotene and alpha-tocopherol it contains.

Because carotenes are destroyed gradually by light and heat, even with optimum harvesting the carotene concentration (on a dry matter basis) in sun-cured forage or hay is lower than in green forage. During protected dry storage, vitamin A activity in feeds decreases an average of 9.5% per month and, therefore, less than one-half, one-third, and one-tenth would remain after 7, 12, and 24 months, respectively (Table 3-3). This is probably a good estimate of the rate of decrease in carotene concentration in feeds. Carotene concentration will decrease much more rapidly if moisture content or temperature during storage are high. Carotene content is also much lower in moldy feed.

Vitamin A Requirement

Expressed in IU of vitamin A per kg of total diet dry matter (and per kg body weight/day) (divide amount/kg by 2.2 to obtain the amount/lb), in horses 300 to 500 (9 to 11) IU is reported to prevent clinical signs of a deficiency and 900 (17 to 19) IU to be sufficient for production of maximum semen quality and quantity and stallion libido. However, 2,000 to 6,000 (60 to 200) IU was needed by foals for optimum growth and maintenance of blood parameters, biochemical parameters, and tissue vitamin A concentrations. As a result, a minimum of 2,000 (30) IU is recommended for maintenance and 3,000 (60 to 80) IU for all other horses. No benefit from additional vitamin A has been demonstrated. However, beta-carotene, in addition to its benefit as a source of vitamin A, may enhance reproductive efficiency, as described below.

The young horse’s growth rate is substantially decreased at a preformed vitamin A intake of 184,000 IU/kg of feed dry matter (4,000 IU/kg body wt/day), and begins to decrease at intakes of greater than 20,000 (400) IU. Although clinical signs due to excessive vitamin A intake are unlikely in mature horses at intakes less than 100 times that recommended, 16,000 IU of preformed vitamin A/kg of total diet dry matter is recommended as the upper safe level for continuous prolonged consumption. When administered for long periods, this amount would be expected to substantially increase liver stores but not saturate liver storage capacity and, therefore, not result in above-normal increases in plasma vitamin A concentrations.

Beta-Carotene’s Effect on Mare Reproduction

Beta-carotene, because of its role as an antioxidant and in controlling progesterone secretion by the corpus luteum, may impair the mare’s reproductive ability, if deficient. Although beta-carotene in hay may be sufficient to provide adequate vitamin A, it may not be sufficient to maintain high plasma beta-carotene concentration and ovarian storage, and to maximize reproductive ability. Horses on green pasture have plasma beta-carotene concentrations 8 to 13 times higher than those fed hay and grain.

Beta-carotene supplementation to both cows and mares not grazing green grass has been reported by some to improve ovarian activity, produce earlier and stronger periods of estrus, improve conception rates, and reduce embryonic mortality; others report no benefit for either mares or cows. However, beta-carotene given orally would be expected to be of little benefit since much of what is ingested is split into vitamin A upon absorption. Beta-carotene availability is also low in conventional beta-carotene preparations because apparently it is present in large-drop-let form. Beta-carotene’s bioavailability is greatly enhanced in emulsified products (such as Equate, BASF Corp, Parsippany, NJ 07054).

A significant benefit of injecting mares and sows with an emulsified preparation of beta-carotene has been reported. In one study, conception rates in 155 randomly selected Thoroughbred mares on 6 farms near Ocala, Florida, injected intramuscularly with beta-carotene (10 ml) on the second or third day of estrus, and again 2 to 3 days later, during April was 91.6% versus 67.6% in 108 mares on the same farms not injected. No localized swelling or adverse reactions to the injections were observed. The administration of a highly bioavailable beta-carotene preparation may, therefore, be of significant benefit, particularly for mares receiving forage with little or no green color. However, it may be of much less or no benefit for mares on green pasture forage or consuming hay containing a significant amount of green color and, therefore, high amounts of beta-carotene.

Vitamin A Imbalances

Vitamin A Occurrence

If the mature horse consumes fresh green forage for a period of 4 to 6 weeks, it will saturate its liver-storage capacity for vitamin A and thus will have sufficient vitamin A to meet its needs for 3 to 6 months, although it usually takes at least a year before mature adults’ vitamin A reserves become depleted. However, a longer period of time without green forage or supplemental vitamin A may result in a vitamin A deficiency, sufficient to cause a clinical effect.

The effects of a vitamin A deficiency most commonly occur in the foal. Vitamin A, like all fat-soluble vitamins, is poorly transported across the placenta. As a result, regardless of the amount of these vitamins consumed by the mare, the foal is deficient in them at birth. Colostrum contains high quantities of vitamins A, D, and E, providing the mare has adequate quantities of these vitamins available. If she does not, or if the foal doesn’t receive adequate quantities of colostrum or has enteritis, which may decrease vitamin A absorption, the deficiency persists.

Excess, like inadequate, vitamin A is harmful. However, just as vitamin A deficiency and its effects don’t occur until hepatic storage is depleted, vitamin A toxicosis and its effects don’t occur until hepatic storage is exceeded. Nor does vitamin A toxicosis occur as a result of excess carotene intake, probably at least in part because carotene’s conversion to vitamin A decreases with increasing carotene intake. Thus, since plant source feeds don’t contain preformed vitamin A, vitamin A toxicosis occurs only as a result of vitamin A supplementation sufficient to exceed hepatic storage capacity.

Vitamin A Imbalance Effects

A vitamin A deficiency is characterized and suggested by excessive tearing and night blindness (Fig. 3-1). The only other known cause of night blindness in horses is a non-nutritionally related night blindness present from birth that occasionally occurs primarily in Appaloosas. These horses show apprehension to darkness and seek light; other signs of vitamin A deficiency are not present. Their eyes are free of ophthalmic lesions, whereas with vitamin A deficiency, the corneas may appear cloudy. In addition, although night blindness may develop, it is not present at birth in the vitamin A-deficient foal.

Fig. 3–1. Excessive tearing caused by vitamin A deficiency. (From Evans, J. W., Borton, A., Hintz, H. F., and Van Vleck, L. D.: The Horse. W.H. Freeman and Company, 1977.)

Although these eye abnormalities are characteristic of a vitamin A deficiency, they are observed only if the deficiency is sufficiently prolonged and severe. Earlier, and generally more commonly observed although less diagnostic, signs include reduced feed intake and growth rate; a rough, dry, dull, brittle, and long hair coat; and in foals an increased incidence and severity of respiratory and diarrheal diseases. Additional clinical signs in foaling mares include reduced fertility, abortion, and endometritis. The same hair coat changes occur with vitamin A toxicosis and protein deficiency as well as with inadequate feed and, therefore, inadequate protein, calorie, and vitamin A intake. Vitamin A-deficient stallions may have decreased libido and soft, flabby testicles. Foals born to vitamin A-deficient mares may be weak at birth. Although similar statistics aren’t available for foals, the effect of vitamin A deficiency on respiratory and diarrheal diseases has been well documented in children. In one study, mortality was increased fourfold, and these diseases were threefold higher in children with a mild vitamin A deficiency than in those not deficient. Supplementing these children with vitamin A reduced childhood mortality by more than 30%.

Additional effects of a vitamin A deficiency include: sublingual salivary gland abscesses, impaired conception, convulsive seizures, progressive weakness, and declines in plasma, liver, and kidney vitamin A concentrations.

A vitamin A deficiency has not been identified as a clinical cause of skeletal problems in horses. However, in other species, a severe vitamin A deficiency increases bone growth and cause abnormal bone remolding, resulting in a reduced medullary cavity. Bony foramina fail to enlarge to accommodate the spinal cord, optic nerve, and cranial nerves which pass through them. This causes compression of these nerves, which may result in posterior incoordination, convulsions or paralysis, deafness, and blindness. Vitamin A deficiency is reported to be the major cause of blindness in children throughout the world, and, after protein and calorie deficiencies, to be the next most common nutritional disease (excluding obesity) occurring in people worldwide.

Some of the effects of a vitamin A deficiency also occur as a result of vitamin A toxicosis. Ponies 4 to 9 months old fed diets providing either less than 22 or greater than 4,000 IIJ of vitamin A/kg of body weight daily (800 or 130,000 IU per kg of total diet dry matter, respectively) gained 20 to 30% less weight, grew 43% less in height, and had duller hair coats and lower hematocrits, number of red blood cells and plasma albumin, cholesterol and iron concentrations than those receiving 40 IU of vitamin A/kg of body weight daily (1,450 IU/kg of total diet dry matter).

Prolonged feeding of excess vitamin A may also cause bone fragility, increased bone size, scaly skin, teratogenesis, and decreased blood clotting, which may result in internal hemorrhage. Severe toxicosis (40,000 IU/kg of body wt/day) produces decreased feed intake and unthriftiness by 15 weeks and, shortly thereafter, rough hair coats, poor muscle tone, and depression. By week 20, there is a loss of large areas of hair and the outer layer of skin, periodic incoordination, and severe depression, with much time spent lying on their sides, with a failure to respond to external stimuli, and death shortly thereafter. Degeneration, fatty infiltration, and reduced hepatic and renal function also typically occur as a result of vitamin A toxicosis. Vitamin A toxicosis also causes microphthalmia, crooked legs, and cleft palates.

In the growing horse a low red blood cell count and low plasma albumin and cholesterol concentrations are characteristic of both a mild vitamin A deficiency and excess sufficient to decrease growth rate, often without causing other clinical signs. If either an inadequate or excessive vitamin A intake is suspected, or if the values for these three parameters are reduced, procedures should be taken to evaluate vitamin A intake.

A total vitamin A concentration of less than 10 µg/dl indicates vitamin A deficiency and greater than 40 to 60 µg/dl an excess, although clinical signs of vitamin A toxicosis are unlikely to occur until concentrations exceed 100 µg/dl. However, plasma vitamin A concentrations in the normal range are poorly correlated with either intake or liver stores.

Like other effects of a vitamin A imbalance, substantial changes in the plasma vitamin A concentration do not occur until liver storage capacity is either nearing depletion or being exceeded.

Since the liver can store sufficient vitamin A to meet all of the horse’s vitamin A needs for 3 to 6 months, a horse would need to continually consume a diet providing inadequate, or excessive, vitamin A for many months to years before its vitamin A storage capacity would be depleted, or exceeded, and, therefore, its plasma vitamin A concentration would move outside the normal range.

Vitamin A Imbalance Prevention and Treatment

If a forage, hay or pasture, without a significant amount of green color is being consumed for more than a few months, it is best to give a balanced vitamin supplement such as that given in Table 3-5. An inadequate intake of both vitamins A and E is likely. A sufficient amount of vitamin supplement should be given to the growing, pregnant, or lactating horse to provide 60 IU of vitamin A/kg body wt/day or 3,000 IU/kg of total diet dry matter (27 or 1,365/lb), and for other horses 30 and 2,000 IU, respectively (14 and 900 lb).

Instead of adding vitamin A to the diet, a water-soluble emulsion of vitamin A may be given intramuscularly or subcutaneously at a dosage of 6,000 to 7,000 IU/kg (2,700 to 3,200 IU/lb). This amount will saturate the liver’s storage capacity and, therefore, does not need to be repeated for at least 3 months. Injecting more than four times this amount, or prolonged feeding of more than 5 to 10 times the amount recommended, may be harmful.

Vitamin A toxicosis is prevented by not giving more than the recommended amounts of vitamin A, and is treated by removal of excess vitamin A from the diet. If death is avoided, recovery from vitamin A toxicosis occurs rapidly. However, there may not be complete resolution of some changes.

VITAMIN D

Forms and Sources

Ultraviolet rays from sunlight convert 7-dehydrocholesterol, which is synthesized in the body, to vitamin D₃ (cholecalciferol) in the skin, and in the dead leaves of plants, they convert ergosterol to vitamin D₂ (ergocalciferol). This occurs, although more slowly, even during cloudy, overcast days, but not if the sunlight passes through glass. Glass blocks ultraviolet rays. Chlorophyll in living plants also blocks out ultraviolet rays. Thus, vitamin D₂ is present in plants after they have been cut and exposed to sunlight, and in the dead leaves of living, insolated plants. One IU of vitamin D (absence of a subscript indicates either vitamin D₂ or D₃) is equal to 0.025 µg of crystalline vitamin D.

The “sunshine vitamin,” either ingested or produced in the skin, is stored and converted to 25-hydroxy vitamin D (25-OH-D) in the liver. This compound is transported to the kidney, where it is further hydroxylated to either the most active form—1,25 dihydroxy vitamin D (1,25 (OH)₂D)—or calcitrol if needed; or if not needed, it is converted to the more inactive form 24,25(OH)₂D. The 25-OH-D₃ form is 2 to 5 times, and the l,25(OH)₂ D₃ is 5 to 10 times, more potent than vitamins D₂ or D₃. Vitamin D₃ is reported to be more potent and absorbed preferentially to vitamin D₂ by horses as well as by cattle and swine.

Functions of Vitamin D

The only function of vitamin D is to assist in maintaining the plasma calcium concentration ([Ca]_p). It accomplishes this by interacting with parathyroid hormone (PTH) and calcitonin.

While l,25(OH)₂D is the primary “effector” in this system. PTH is the primary “controller,” with calcitonin playing an assisting role. For adequate control of calcium and phosphorus metabolism, adequate amounts of all elements in the system must be present. This includes calcium, phosphorus, vitamin D, PTH, and calcitonin. When there are deficiencies or excesses of any of these substances, skeletal diseases occur.

Vitamin D Requirement

If the horse receives sun-cured hay not stored for more than one season, or dormant sun-cured pasture forage, or is outside unshaded for an average of several hours daily, its vitamin D needs will be met. In this case, supplemental vitamin D is not needed, is not of any known benefit, and is not recommended. However, stabled horses not allowed access to direct sunlight for periods in excess of several months should have in their total diet dry matter 800 IU of vitamin D/kg during growth, pregnancy, and lactation, and 300 IU/kg during all other periods (365 or 135 IU/ lb, respectively). In IU/kg (or/lb) of body weight, these amounts are equivalent to 24(11) for rapid growth and early lactation, 16(7) for late pregnancy, and 6(3) for maintenance. Sun-cured hay initially contains 2,000 II! of vitamin D₂/kg dry matter (or 900/lb; Appendix Table 3). However, the activity of vitamin D, like other vitamins, decreases during storage. During protected dry-feed storage, vitamin D activity decreases an average of 7.5%/ month; therefore, only 39% and 15% would remain after 1 and 2 years, respectively (Table 3-3) Thus, hay stored for more than one season may contain inadequate vitamin D to meet the horse’s requirements, which is of no consequence for the horse that receives an average of a few hours or more of sunlight daily. However, for those that don’t, the amount of vitamin D recommended above should be given. Vitamin D may be preferably added to the diet or it may be given as an injection. Vitamin D₂ and D₃ have a 6 to 18-week effect, versus 4 to 12 weeks for 25-OH-D3 and 1 to 6 days for l,25(OH)₂D. Thus, if vitamin D is injected, it should not be given any more frequently than every 6 to 18 weeks, and then only if needed.

Vitamin D Administration for Skeletal Diseases

Since vitamin D increases intestinal calcium and phosphorus absorption and bone mineralization, it is occasionally given to growing horses to assist in the treatment or prevention of skeletal disease. Skeletal disease in the growing horse, as discussed in Chapter 16, is associated with numerous nutritional imbalances, most commonly either calcium or phosphorus deficiencies or both, but not vitamin D deficiency. Although high amounts of vitamin D can to some extent compensate for low dietary calcium and phosphorus by increasing their intestinal absorption, unless the situation described above, in which giving vitamin D is recommended, is present, vitamin D administration is unlikely to be of more than minimal, if any, benefit. No amount of vitamin D will compensate to any significant degree for inadequate calcium or phosphorus, or an improper Ca:P ratio, in the diet. Dietary calcium and phosphorus imbalances can be treated and prevented only by ensuring that the diet contains the proper amount of these minerals by evaluating and formulating an adequate diet as described in Chapter 6.

Vitamin D Deficiency

A vitamin D deficiency in most species results in rickets in the young and inadequate bone mineralization in the adult. A highly stable bone-cartilage matrix that is un-calcified and difficult to resorb is produced. This results in cartilage cells not degenerating, and a buildup of large cartilage cells, which produce more nonresorbable bone matrix. A palpable and observable broadening of the bone growth plates because of to the presence of uncalcified cartilage and bone matrix occurs. In severe or chronic cases, affected animals are reluctant to stand and do so with difficulty and pain. The bones become soft and flexible, resulting in bowed legs. However, often the most striking feature of the condition is emaciation. If the condition is treated early, all effects are readily reversed.

The skeletal effects of vitamin D deficiency, either naturally occurring or experimentally induced, have not been reported in horses. Ponies 3 months and 9 months of age deprived of all sunlight for 5 months and with no vitamin D added to the diet did not develop any of the clinical signs of rickets. However, there was a decrease in appetite, feed intake, growth, bone ash content, bone cortical area, and bone breaking strength. No difference in feed efficiency or in plasma calcium, phosphorus, or magnesium concentrations were observed as compared with ponies deprived of sunlight and given vitamin D daily or those that were outside with no vitamin D added to the diet. In addition, bone growth plates were irregular, widened, and poorly defined on radiographs, and were late in closing in the ponies deprived of sunlight and not given vitamin D. There was no difference in any of these parameters between ponies deprived of sunlight and given vitamin D, and those outside but not given vitamin D.

Vitamin D Toxicosis

Occurrence of Vitamin D Toxicosis

Vitamin D toxicosis is the most common of all vitamin toxicoses. It occurs as a result of improperly formulated vitamin D-supplemented feeds, administration of excessive oral or injected vitamin D, or the ingestion of plants containing vitamin D glycosides (Table 18-8), which are found primarily in subtropical areas of the world but also Florida, Texas, and southern California. Most commercially available vitamin D, both injectable and for oral administration, is synthetic vitamin D₃. Vitamin D₃ is used preferentially and, therefore, is more active and toxic than vitamin D₂ for horses, as it is for most animal species evaluated.

Excess vitamin D is cumulative. It may take several weeks or longer for its effect to become evident. A maximum upper safe level of 2,200 IU of vitamin D₃/kg (1,000/ lb) of total diet dry matter is recommended for continual long-term consumption. This is equivalent to 40 to 60 IU/ kg (18 to 27 IU/lb) of body wt daily. This amount would not be expected to increase plasma 25-OH-D₃ levels above normal, which is a sensitive indicator of vitamin D₃ excess. A vitamin D₂ intake of more than 10 times this level is probably safe. In addition, greater than 10 times this amount of vitamin D₃ is probably not harmful for periods of less than 60 days.

Vitamin D Toxicosis Effects

Vitamin D in excess performs its normal functions in the body, but does so in excess, thus stimulating excessive calcium and phosphorus absorption and calcium deposition. Calcium deposition occurs in various soft tissues, especially heart walls and valves, walls of large blood vessels (e.g., pulmonary arteries and aorta), and also the kidney, gastric mucosa, salivary glands, and diaphragm.

Vitamin D toxicosis results in the following clinical signs and alterations given in the order of their occurrence.

1. Decreased exercise tolerance and performance.

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