Zinc for Animals

Zinc is widely distributed throughout the body and plays an essential role in many body processes. Radioactive zinc given orally or intravenously reached peak concentrations in the liver within a few days, but concentrations in red blood cells, muscle, bone and hair do not peak for several weeks. Zinc is present in many enzyme systems that are concerned with the metabolism of feed constituents. For example, zinc is a constituent of carbonic anhydrase, carboxypeptidase A and B, several dehydrogenases, alkaline phosphatase, ribonuclease and DNA polymerase. Zinc is required for normal protein synthesis and metabolism, and it is also a component of insulin so that it functions in carbohydrate metabolism. Because zinc plays so many important roles in the body, it is required by all livestock and poultry (Table 22).

Class of Animal	Zinc Requirement in total Diet (ppm)	Toxic Level in Total Diet (ppm)
Beef Cattle	30	500³
Dairy Cattle	23-63²	300-1,000
Swine	50 (50-100)²	2,000-4,000²
Horses	40	Over 700
Sheep	20-33	750³
Goats	45-75	750⁴
Chickens	40-50	800-3,000
Turkeys	40-75	4,000

Absorption of zinc occurs throughout the small intestine and usually ranges from 5% to 40% of the intake. Transfer of zinc out of the intestinal mucosal cells to the plasma is regulated by metallothionine. Zinc absorption is reduced whenever diets are high in calcium or phytate (215). Common sources of supplemental zinc include zinc sulfate, zinc oxide, zinc chloride, zinc carbonate and zinc chelates.

A severe deficiency of zinc in young calves results in parakeratosis (a condition that resembles mange). The nose and mouth become inflamed with sub-mucosal hemorrhages. The animal also develops an unthrifty appearance, a roughened hair coat and joint stiffness. A mild zinc deficiency in finishing cattle results in lowered weight gains, but they show no clinical signs of a deficiency (85, 157). Excessive salivation is an early sign peculiar to ruminants. It may be caused by a reluctance to swallow the large amount of salvia that is normally produced (228). Hypogonadism is a common occurrence in zinc deficient bull calves.

Many recent studies have shown zinc to be essential to maximum immune function in stressed feedlot cattle. Texas researchers (208) reported that when steer calves were challenged with virulent infectious bovine rhinotrachetis (IBR) virus, serum zinc levels decreased significantly. The same author showed that during a natural outbreak of bovine respiratory disease, serum zinc levels were lowest at the time of peak morbidity. Substantial losses in immune capacity can occur due to inadequate zinc intakes before typical zinc deficiency symptoms appear (209).

A USDA study in Idaho by H. R. Mayland and co-workers showed that cows and their suckling calves grazing mature dry forage supplemented with zinc resulted in calves gaining 6% more weight (90). The forage being fed contained less that 20 ppm zinc. In cattle zinc plays a critical role in the proteolytic enzyme systems associated with muscle protein turnover. Muscle protein accretion decreased when supplemental zinc was removed for 21 days and then returned to normal after 14 days of supplementation (307). Some foreign scientists have reported signs of zinc deficiency in cattle grazing forages containing 20 to 30 ppm zinc. Missouri researchers drew blood on 529 feeder calves to evaluate zinc status. They found that 2.4% of the calves were zinc deficient and 24.4% were marginally deficient (324). In a recent Tennessee study, 83.1% of the 1021 forages samples analyzed were considered deficient or marginally deficient in zinc (293). Florida researchers have reported zinc deficiencies in four regions of the state (125). One must keep in mind that forages may differ in zinc level and availability and that the stage of maturity may also affect zinc availability. Data of Emanuele and Staples (210) showed that the maximum availability of zinc in bermudagrass and alfalfa was only 62.1% and 79.4%, respectively. The Idaho, Florida and other studies indicate a need to be concerned about the adequacy of zinc in cattle grazing forages, especially with mature, dry forages or hay made from them.

The zinc requirement for normal beef cattle appears to be between 20 and 40 ppm in the total diet. However, this requirement probably doubles during time of stress. Hutcheson (208) suggests that dietary zinc should be increased to approximately 80 ppm for stressed and sick feedlot cattle due to decreased feed intake and increased excretion of body zinc stores. Excess calcium in the diet may also increase the zinc requirement. The pig, for example, may need at least twice as much zinc if excess calcium is consumed in the diet. The influence of calcium level on zinc requirement is probably less in ruminants than non-ruminants (337). Zinc toxicity is seldom a problem. However, high levels of zinc caused harmful effects in beef cattle fed 900 ppm, which results in reduced gains and feed utilization (157). The 1984 NRC publication (157) gives 500 ppm as the maximum tolerable level.

Lowered feed intake is one of the first changes observed in a zinc deficiency. The cattle grow slower due to a decreased feed intake and less efficient feed utilization. Other symptoms in a severe zinc deficiency are skin parakeratosis (usually most severe on the legs, neck and head), hair loss, unthrifty appearance, stiffness of joints, teeth gnashing, retarded testicular growth and excessive salivation. Reduced reproductive performance has been observed in both males and females fed zinc deficient diets (211). Another effect of a zinc deficiency is a failure of wounds to heal normally. In most cases, when a zinc deficient animal is given zinc, there is a dramatic and quick recovery. Improvements are observed within 24 hours after supplementation.

The estimated zinc requirement for dairy cattle is 40 ppm in the diet (156). There may be certain conditions or an interrelationship with other nutrients that might increase zinc needs. For example, a small percentage of Dutch-Friesian calves are born with an apparently inherited defect that causes a very severe zinc deficiency which can be temporarily corrected by very high amounts of zinc. Whether this means there are genetic differences affecting zinc needs is not well established. A review of the various experiments conducted on the zinc requirements of dairy cattle and the levels needed in each one indicate there is considerable variation in the requirements obtained. However, factors other than genetics are also involved (91).

Studies on excess zinc levels indicate that lactating dairy cows fed 1,279 ppm zinc in the diet did not experience reduced performance (212). Growing cattle fed 900 ppm zinc exhibited decreased weight gains and decreased feed efficiency. Based on these and other studies, the 1980 NRC publication, Mineral Tolerance of Domestic Animals, suggest that 1,000 ppm zinc in the diet is the point at which adverse physiological effects are observed (97).

Regardless of the level of zinc fed previously, cattle fed a severe zinc deficient diet may develop a deficiency within a few weeks. In other words, body stores of zinc do not last very long. The average zinc content of milk is about 4 ppm, but there is considerable difference among cows in the level of zinc in their milk. Milk zinc concentrations will decrease rapidly in response to a dietary deficiency (213).

The symptoms of zinc deficiency are reduced appetite and growth rate, skin lesions (parakeratosis) that look like mange, diarrhea, vomiting, and death in severe cases. Borderline deficiencies produce decreased appetite and growth in some animals, while others may show a fading or bleaching of the hair coat. A decrease in litter size and weight of pigs occurs with the sow, and retarded testicular development occurs with the growing boar. The zinc deficient pig also shows reduced tissue and blood zinc levels and reduced blood alkaline phosphatase activity (87).

Zinc is also critical to immune function in the pig. Miller (214) reported that zinc deficient pigs died following an intraperitoneal injection with Salmonella pullorum antigen, while there was no mortality in pigs receiving adequate dietary zinc and challenged similarly. One mechanism by which a zinc deficiency can impair the immune system is by causing atrophy of the thymus gland. This was demonstrated dramatically in the Miller study (214) where pigs fed zinc adequate diets (100 ppm) had thymus glands weighing 51 grams while the thymus glands of pigs fed 12 ppm zinc weighed only 2 grams. The small intestine is an organ that plays a key role in immune function. Louisiana State researchers showed that adding an additional 100 ppm zinc from zinc sulfate to a control diet containing a 100 ppm zinc during gestation increased the increased the jejunal villus height of piglets at 28 days of age (359). The mechanism by which zinc level consumed by the mother influences gut development of her offspring a month after birth is being investigated.

A pig with parakeratosis responds very quickly and dramatically to zinc. Appetite increases immediately and an improvement in skin condition and weight gain is quite obvious within a week. The pigs soon recover from the skin lesions and other symptoms and may be completely recovered within one month.

The requirement for zinc by the pig is about 50 ppm in the diet. If the calcium level in the diet is excessive, the addition of 50 to 100 ppm zinc to the diet will not always completely prevent the growth depression and poor feed conversion associated with parakeratosis, although it will prevent the typical skin lesions. Therefore, under some conditions, a level of 100 to 150 ppm zinc is needed. However, in most cases, a level of 100 ppm zinc should be adequate. The level of calcium that causes parakeratosis will vary considerably. Sometimes a high calcium diet that supposedly should cause parakeratosis does not do so, and sometimes parakeratosis occurs with a low level of calcium (87, 92).

The zinc in soybean meal, cottonseed meal, sesame meal and other plant protein supplements has low availability to the pig (and also to the chick). The reason for this is these supplements are high in phytic acid, which combines with zinc to form zinc phytate, this complex is insoluble in the intestinal tract and cannot be absorbed. Therefore, the zinc in plant protein concentrates is less available than in animal protein supplements, such as meat meal and fish meal which contain no phytic acid. For example, the zinc requirement of the pig fed soybean meal is 50 ppm, whereas it is 18 ppm for pigs fed casein (animal protein) as the source of protein in the diet (87).

There is no danger in feeding pigs up to 150 ppm zinc in the diet (which occasionally is done) since over 1,000 ppm has been fed without any harmful effects. However, a level of 2,000 ppm zinc in the diet of the pig can causes toxic effects including growth depression, enteritis, arthritis, gastritis and hemorrhage in the axillary spaces (87). The form and bioavailability of the zinc source can greatly influences the toxic dose. For example, several experiments have shown a performance benefit from feeding high levels of zinc oxide to weanling pigs. Poulsen (229) reported that feeding 28-day old weanling pigs diets containing 2500 ppm zinc from zinc oxide improved gains and feed efficiency. A supplement of 2500 ppm zinc for two weeks post-weaning reduced the incidence of diarrhea by up to 50%. Smith (230) studied the effect of replacing corn starch with zinc oxide to provide 165, 1000, 2000, 3000, and 4000 ppm zinc in the diet on the performance of piglets weaned at 13 days of age. From 0 to 14 days postweaning, increasing the zinc oxide level linearly increased feed intake and feed efficiency. However, the 4000 ppm zinc addition began to depress performance as the pigs got older. The authors concluded that maximum performance was achieved if 4000 ppm zinc was fed from day 0 to 14, and 2000 ppm from day 14 to 28 postweaning. It is unlikely that these performance responses were due to the high dietary zinc improving the nutrient status of the piglets. This was confirmed recently when it was shown that supplemental zinc whether in the form of zinc oxide or in an organic form, was not as efficacious for improving gain and feed intakes as 2000 ppm zinc from zinc oxide (358). Most nutritionists believe that the high concentrations of zinc from zinc oxide are inhibiting the growth of pathogenic bacteria that commonly affect the early-weaned pig.

The next question to consider is whether the responses to these high levels of zinc are additive to the wide spread practice of feeding 250 ppm of copper. A cooperative study involving 12 universities was reported to address this issue (275). Their summary showed that growth and feed efficiency was improved in nursery pigs when fed either 3,000 ppm of zinc or 250 ppm of copper from copper sulfate. However, no additive or synergistic benefit from feeding the combination was observed.

Monitoring the zinc status of pigs by measuring the zinc concentration in the blood serum or plasma has been a common practice in the past. However, recent research shows that blood zinc concentrations may not be a very sensitive diagnostic tool. Wedekind (231) reported that blood concentrations of zinc were higher in unfed animals than fed animals. The difference actually widened as zinc intakes decreased, to the point that unfed animals had plasma zinc levels twice that of fed animals on the same low-zinc diet. Assessing zinc status is difficult because there are no effective tests for marginal zinc deficiency. In general, if plasma zinc is below 0.4 mg/liter, pigs are considered deficient in zinc.

The symptoms of a zinc deficiency are similar to those obtained with cattle, swine and sheep. A zinc deficiency in the foal results in reduced appetite and growth rate, parakeratosis with considerable lesions in the feet, legs and head and loss of hair. The horses also show reduced tissue and blood zinc levels and reduced blood alkaline phosphatase (154).

The zinc requirement of the horse is approximately 40 ppm (154). However, some animal scientists recommend the use of 100 ppm zinc in the total diet because many horses will be fed higher levels of calcium than required. One hundred ppm will ensure an adequate level of zinc in the diet and provide a safety margin against the many factors that affect zinc needs. It will also protect the horse against loss of zinc, which may be tied up by the phytate phosphorus in soybean meal and other plant protein supplements. Moreover, most owners like to have their horses with beautiful looking skin and hair which makes it essential that zinc levels in the diet be adequate (98).

Research suggests that zinc along with copper and calcium play key roles in the prevention of Developmental Orthopedic Disease (DOD). Anderson (297) defined DOD of the young horse as any disturbance in the changing of the cartilaginous precursor of the skeleton to functional bone. For optimal bone mineralization in the young growing horse, 60-80 ppm zinc are recommended (298).

The danger of feeding excess zinc is low, since the feeding of 700 ppm in the diet was not detrimental to mares or their foals. Foals fed 20,000 ppm zinc in the diet, however, developed enlarged epiphyses followed by stiffness, lameness and increased tissue zinc levels (154).

Zinc deficiency in lambs results in a lack of appetite, reduced growth, slipping of wool, swelling around the eyes and hooves, excess salivation, general listlessness, impaired growth of testes and cessation of spermatogenesis (155). Loss of appetite is the first sign of a zinc deficiency in growing lambs. Recent studies have shown that lambs switch from meal eaters to nibblers (232) as they become zinc deficient. Pair-feeding studies show that many of the signs of a severe zinc deficiency are secondary to a loss in appetite. In a USDA study in New York, ewes were fed a low-zinc diet during the last third of gestation and for the first six weeks of lactation (99). The zinc deficiency caused a few deaths, a continuous loss in body weight during lactation and development of skin lesions and frothy saliva. The rapid deterioration of the ewes after lambing suggests the zinc stores were depleted by the end of pregnancy and the marginal zinc levels may have contributed to the deaths that occurred. A recent study showed that 7 of 30 ewes fed a low-zinc diet aborted, reabsorbed or delivered mummified and deformed lambs, while the other 23 ewes delivered lambs that were 20% smaller than the controls (153). Feeding a diet containing only 3 ppm zinc during pregnancy reduced survival of the newborn lambs and caused pregnancy toxemia in the ewes as a result of anorexia (234). White (233) showed that zinc-deficiency-induced anorexia caused reduced secretion of gonadotrophin-releasing hormone from the hypothalamus of ram lambs. This will lead to impaired fertility in the ram.

The requirement of zinc for sheep is 20-33 ppm in the diet. The maximum tolerable level in the diet is 750 ppm (155). Excess zinc will cause a copper deficiency.

Zinc deficiency in goats includes reduced feed intake, weight loss, parakeratosis (mange-like condition), stiffness of joints, excessive salivation, swelling of the feet and horny overgrowth, small testicles and low libido (120).

A level of 45 to 75 ppm zinc should be used in the total diet of goats until their zinc requirements are met.

Zinc deficiency causes growth retardation and abnormal feather development in poultry. Feather fraying occurs near the end of the feather. The severity of the fraying varies from almost no feathers on the wings and tail to only slight defects in the development of some of the barbules and barbicels. The hock joint may become enlarged. The long bones of the legs and wings also become shortened and thickened with a zinc deficiency. Other symptoms include scaling of the skin, especially on the feet, loss of appetite, reduced efficiency of feed utilization, and mortality in severe cases. Zinc deficiency in the breeder diet reduces egg production and hatchability. Embryos produced in zinc deficient eggs show a wide variety of skeletal abnormalities in the head, limbs and vertebrae. The hatched chicks also may not stand, eat or drink (95, 141). Proper zinc supplementation has proven to be important in reducing early mortality of turkey poults (306).

The 1984 NRC publication, Nutrient Requirements of Poultry, recommends a level of 40-75 ppm zinc in various poultry diets (141). This publication indicates that the toxic level of zinc varied from 800 to 4,000 ppm in the diet (141).

There is a lack of quantitative data on the zinc requirements of small animals. In some cases the latest National Research Council publications give suggested levels to use or levels of zinc that have been used successfully. These levels in ppm in the total diet are as follows: dogs, 60 to 90; cats, 30; fish, 15 to 78; rats, 12; mice, 30 to 58; guinea pigs, 20; hamsters, 9.2 and gerbils, 8.4. These levels can be used as guides until more definitive information is obtained. All animals need zinc in the diet but, in most cases, research has not been conducted to determine how much is needed. In a few instances where some deficiency symptoms were given, there was some similarity to those reported for domestic livestock.

Supplemental zinc is usually added to animal diets in the form of zinc oxide or zinc sulfate. Recent comparisons of bioavailability in chicks suggest that feed grade zinc oxide has only 44-78% the availability of zinc sulfate when added to purified (235) or practical (236) diets. A recent comparison of availabilities of zinc sources for pigs in corn-soy diets ranked zinc sulfate > zinc methionine > zinc oxide > zinc lysine (237).