Vitamins

The fat-soluble vitamins are important in goat nutrition, as they are in the feeding of other domestic animals and humans. Water-soluble vitamins other than thiamine and niacin are generally ignored when formulating caprine rations.

Vitamin A

Beta-carotene is the standard dietary precursor of vitamin A, although some other carotenoids also have biologic activity. Previously (NRC 1981b), 1 mg of beta-carotene was judged to be equivalent to approximately 400 IU vita­min A. Currently recommended conversions are 671 IU of vitamin A/mg of beta-carotene and 436 IU∕mg of other common carotenoids such as cryptoxanthine in yellow corn (NRC 2007). As little as 10% of dietary beta-carotene escapes degradation in the rumen. Absorption, metabo­lism, and storage of the remainder require a healthy diges­tive epithelium and liver (Ferrando and Barlet 1978).

Vitamin A can also be expressed as retinol equivalents (REs), where 1 IU = 0.3 μg of retinol. The biopotency of 1 RE for goats is expressed as the vitamin A activity of 1 μg of all- trans retinol, 5 μg of all- trans beta-carotene, or 7.6 μg of other carotenoids with vitamin A activity (NRC 2007). The vitamin A requirement tables in this reference book use the RE unit. The RE can be converted back to IU of vitamin A by multiplying by 3.33, thus 1 RE = approximately 3.33 IU of vitamin A.

Signs of Deficiency

Poor appetite, weight loss, unthrifty appearance with a poor haircoat, night blindness, and a thick nasal discharge have resulted from experimental vitamin A deficiency in goats (Schmidt 1941). Especially in young animals, a defi­ciency predisposes to diarrheal and respiratory disease and to parasitism. To further compound the problem, kids with coccidiosis have an increased vitamin A requirement because of impaired absorption. Adult goats may have a decreased fertility rate related to inadequate steroid hor­mone synthesis (Arellano-Rodriguez et al.

Dietary Recommendations and Supplementation

The NRC applies sheep requirements to goats. According to its 2007 recommendations, the daily maintenance requirement is 31.4 RE/kg bw or 104.7 IU∕kg. The 50 kg goat at maintenance should receive 1570 RE or approxi­mately 5235 IU of vitamin A∕day, while the 90 kg goat needs approximately 9423 IU. To this is to be added 45.5 RE/kg (152 IU∕kg)∕day for late pregnancy and 100 RE/kg (333 IU∕kg) for growing goats. The NRC 2007 additional requirement for lactation is now 53.5 RE/kg and disregards the level of milk production. A simplified recommendation from the French is 5000 IU vitamin A∕kg dry matter (DM) of feed across the board (Morand-Fehr 1981b). Browse and green leafy hays are good sources of vitamin A, while old or weathered hay is a poor source. After six months of stor­age, all beta-carotene in hay has been destroyed (Ferrando and Barlet 1978). Vitamin A palmitate is commonly added to mineral mixes and commercial concentrates. Because vitamin A is fat soluble and stored in the liver and other body fat, the adult goat can tolerate several months of low carotene intake without developing clinical signs of defi­ciency. Vitamin A toxicity does not occur when natural diets are fed, but could occur with mixing errors. A maxi­mum of 6000 μg of retinol/kg bw/day is recommended (NRC 2007).

Colostrum is a very rich source of vitamin A, and before its consumption kids have minimal stores. When kids receive colostrum from does that are primiparous (decreased concentration of vitamin A), or only limited amounts of colostrum, an oral vitamin A palmitate supple­ment is desirable. Injectable vitamin A is less valuable because of rapid peroxidation at the injection site.

Vitamin D

There are two principal forms of vitamin D.

The metabolism of vitamin D3 involves several steps. First, it is carried from the skin or digestive tract to the liver, where it is transformed to 25-hydroxycholecalciferol. Next, it passes to the kidney where a second hydroxylation creates 1,25-dihydroxycholecalciferol. This metabolite acts as a steroid hormone in increasing phosphorus absorption and inducing synthesis of calcium-binding hormone in the intestine. Synthesis of 1,25-dihydroxycholecalciferol is stimulated by any decrease in blood calcium or phosphorus levels and by parathyroid hormone.

Signs of Deficiency

The effect of 1,25-dihydroxycholecalciferol on bone metab­olism is important but complex. It stimulates both the fixa­tion and release of calcium and phosphorus from the skeleton. Young, growing animals raised in dark condi­tions, whose dams were similarly housed and deprived of a vitamin D supplement, develop rickets. Signs include bowed limbs, enlarged joints, stiffness, and a rachitic rosary on the ribs. Growth rate and body condition are poor. Adults deficient in vitamin D develop osteomalacia or osteoporosis, especially if dietary calcium and phospho­rous are not properly balanced. Blood calcium and phos­phorus levels may be decreased, but this is not a consistent finding (Ferrando and Barlet 1978). See Chapter 4 for further discussion of metabolic bone diseases.

Dietary Recommendations and Supplementation

The exact vitamin D requirements for goats have not been determined. A level of 5.6IU/kg bw/day has been recom­mended for both sheep and goats (NRC 2007).

Vitamin D Toxicosis

Excess vitamin D activity from certain toxic plants (Mello 2003) such as yellow oat grass (Trisetum flavescens; Braun et al. 2000) in Europe and day-blooming jasmine (Cestrum diurnum) in the southeastern United States causes calcinosis of tendons and other soft tissues, as dis­cussed further in Chapter 4. The same effect can be had by large overdoses of oral or injectable vitamin D supplements (Singh and Prasad 1989).

Vitamin E

Vitamin E (1 mg dl-alpha tocopheryl acetate = 1 IU) is pre­sent in colostrum, milk, and many natural feeds, especially green forage. Ruminants do not synthesize vitamin E but require it in their diet (Van Metre and Callan 2001). Its main action is as an antioxidant; it stabilizes polyunsatu­rated fatty acids (PUFAs), vitamin A, and various hor­mones and enzymes. Vitamin E and selenium are closely interrelated; a deficiency of one can be at least partially offset by increasing the intake of the other.

Signs of Deficiency

Vitamin E deficiency alone can cause nutritional muscular dystrophy (white muscle disease). This is most likely to occur with feeding of silage or old hay, because the vitamin is lost in storage. Kids may have muscle disease at birth and be too weak to suckle (Kolb and Kaskous 2003). Sudden death related to Zenker's necrosis of heart muscle or dia­phragm may occur, even in kids with normal selenium sta­tus (Byrne 1992). Inhalation pneumonia can also result from muscle weakness of the larynx and pharynx. Affected kids are sometimes noted to cough or have milk run out the nose after drinking.

Adult females may show poor uterine involution and retained placenta. Undesirable milk flavors related to oxida­tion of milk fat might be expected to occur with vitamin E/ selenium deficiency. Ventral edema of Angora goats (see Chapter 3) has also been associated with vitamin E deficiency.

Vitamin E is also very important for optimizing immune responses. Beneficial effects have been demonstrated in ruminants on phagocytosis by polymorphonuclear cells and on cell-mediated immunity (NRC 2007). Obviously, increased incidence or severity of infectious diseases is a very non­specific sign of vitamin E deficiency, but is part of the reason for recent increases in the dietary recommendation.

Plasma vitamin E concentrations of less than 1.5 μmol∕L (65 μg∕dL) in preparturient does and less than 1 μmol∕L (43 μg∕dL) in suckling kids have been associated with increased risk of myopathy (Jones et al. 1988). A normal range in goat serum of 60-150 μg∕dL has been proposed (Puls 1994b; Van Metre and Callan 2001). Note that the blood sample needs to be handled very carefully (no hemolysis, rapid refrigeration, and removal of the plasma or serum from the erythrocytes) if accurate results are to be obtained. Liver vitamin E concentration can also be deter­mined and may better reflect the nutritional status of the animal (Liesegang et al. 2008). A normal caprine liver concentration of greater than 250 μg∕100 g wet weight (Van Metre and Callan 2001) or greater than 2.0 ppm wet weight (Puls 1994b) has been proposed.

Dietary Recommendations and Supplementation

In the absence of selenium deficiency, the daily require­ment of vitamin E for preventing nutritional muscular dys­trophy in preruminant lambs and calves, and presumably kids, was previously given as 0.1-0.3 IU∕kg bw (Ferrando and Barlet 1978).

Vitamin E is oxidized by iron (or copper) in the feed, and thus diets with high iron content may have less vitamin E available. Rapidly growing green plants have a high con­tent of PUFAs and animals on lush pasture also have a higher need for antioxidants such as vitamin E, because of increased incorporation of PUFAs into cell membranes and thus increased susceptibility to lipid peroxidation (Van Metre and Callan 2001). Oil seeds also contain high con­centrations of PUFAs.

The vitamin E content of colostrum depends on the nutrition of the dam during pregnancy. At the end of the winter, when most goats in temperate climates kid, the hay cut the previous year is very low in vitamin E. Supplementation of the pregnant doe is important for optimizing kid health.

Some injectable preparations such as vitamin A and D include vitamin E as an antioxidant to stabilize the other fat-soluble vitamins; the quantity of vitamin E is inadequate for therapeutic purposes. Similarly, some vitamin E∕sele- nium preparations contain relatively little vitamin E. Injectable preparations of vitamin E alone are available, with labeled recommendations of 600-900IU to lambs at birth or weaning and 1200-1500IU to ewes prepartum or at lambing.

B Vitamins

B vitamins are normally synthesized in adequate amounts by rumen microbes and thus supplementation of the adult goat's diet is not required. Colostrum is a good source of B vitamins. Older kids that do not yet have a fully developed rumen may need a dietary source of B complex vitamins, and supplementation of milk replacers is advisable. B vita­mins also should be added to the diet or administered by injection to sick animals and those with poor rumen func­tion or marked change in diet (NRC 1981b). Dietary supple­mentation with niacin is sometimes recommended for prevention of pregnancy toxemia (see below). There is cur­rently no evidence that additional biotin promotes hoof health in goats (NRC 2007). Supplementation of periparturi­ent does with rumen-protected choline may increase milk production, although the effect likely reflects dietary methio­nine availability (D'Ambrosio et al. 2007; Pinotti et al. 2008).

There are two instances in which B vitamin deficiency assumes primary clinical importance. The first is when a cobalt deficiency prevents synthesis of adequate vitamin B₁₂; this is discussed under cobalt requirements. The sec­ond problem is polioencephalomalacia, which can be caused by a thiamine (thiamin, vitamin B1) deficiency and results in severe neurologic signs. In this disease, rumen microbes fail to synthesize adequate thiamine, a toxic fern provides a thiaminase (Pritchard and Eggleston 1978), or, more commonly, an abnormal population of rumen microbes produces a thiaminase (Thomas et al. 1987). An excessive proportion of concentrates to roughage in the ration predisposes to polioencephalomalacia, as described under indigestion and rumen acidosis. In addition to the changes in rumen microbes that occur with grain feeding, decreased rumen pH values optimize the action of bacte­rial thiaminase (Brent 1976). Polioencephalomalacia is considered in detail in Chapter 5.