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Volume 45 | Issue 2 Article 3

1983 Selenium Deficiency in Cattle Marc A. Miller Iowa State University

James R. Thompson Iowa State University

Follow this and additional works at: https://lib.dr.iastate.edu/iowastate_veterinarian Part of the Inorganic Chemicals Commons, and the Large or Food Animal and Equine Medicine Commons

Recommended Citation Miller, Marc A. and Thompson, James R. (1983) "Selenium Deficiency in Cattle," Iowa State University Veterinarian: Vol. 45 : Iss. 2 , Article 3. Available at: https://lib.dr.iastate.edu/iowastate_veterinarian/vol45/iss2/3

This Article is brought to you for free and open access by the Journals at Iowa State University Digital Repository. It has been accepted for inclusion in Iowa State University Veterinarian by an authorized editor of Iowa State University Digital Repository. For more information, please contact [email protected]. Selenium Deficiency in Cattle Marc A. Miller, BS, DVM* James R. Thompson, DVM, MS**

SUMMARY A nonselenium-dependent GSH-Px is also Our knowledge of selenium deficiency as a present in tissue. In domestic animals the cause of animal disease has increased since amount of this enzyme varies as well as its tis­ 1973, when the role of selenium (Se) in glu­ sue location. In bovine, the liver, lungs, tathione peroxidase was discovered. 1 G1u­ adrenal glands, testes, and kidneys contain tathione peroxidase (GSH-Px) works with vi­ both enzymes. However, in the spleen, eryth­ tamin E in the cytosol to prevent cell rocyte, brain, thymus, adipose tissue, cardiac membrane damage. Selenium deficiency muscle, and skeletal muscle, only Se-depend­ causes nutritional myopathy (white muscle dis­ ent GSH-Px is found. 9 The presence of only ease) in young calves and yearlings. It is also Se-dependent GSH-Px helps to explain the lo­ implicated in a sudden death syndrome in cation of lesions found in Se-deficient animals. calves less than three months old from acute myocardial degeneration. In adult cattle it is AVAILABILITY associated with muscle disease, retained pla­ Selenium in soil is found in two forms: sele­ centas, and infertility. Se-deficiency diseases nate and selenite. The selenite form is less have been reported in Canada, Great Britain, available for plant uptake and is found in New Zealand, Sweden, and the United States. 2 acidic, poorly drained soils. Plants grown on BIOLOGICAL AND PHYSIOLOGICAL this type of soil are likely to be Se-deficient. ROLE OF SELENIUM Moreover, good weather and the proper fertil­ Selenium, in conjunction with vitamin E, izer content of soil provide for a lush growth, prevents cell membrane damage due to excess further reducing Se content by dilution among organic hydroperoxide and hydrogen peroxide the abundant growth. in the cytosol. These peroxides can react with Surveys of crops grown in the United States and destroy cell membrane components by ox­ provide data needed to map areas of Se-defi­ idation. While vitamin E acts directly, selenium ciency. Deficient areas in the United States in­ works as part of GSH-Px. 4 This enzyme cata­ clude the southeast, northeast, midwest, and lyzes the following reaction: 3, 4 Reduced Glu­ far northwest. 1o These areas of low plant sele­ tathion + H 20 2 GSH-Px Oxidized Glu- nium (less than .05 ppm) correlate closely with the occurrence of Se-deficiency diseases. tathione + H 20. Through its metabolism of hydroperoxides, In animal diets the availability of Se for ab­ GSH-Px may be involved with the following: sorption is important, since no mechanism for the synthesis of various prostaglandin deriva­ its storage has been recognized. Animals are tives; the normal function oflymphocytes, neu­ able to utilize both the inorganic salts (selenite, trophils, and macrophages; and maintenance selenate) and organic forms (plant, animal) of Se. ll The organic form of plant origin has the of erythrocyte integrity. 2,5,6,7 Moreover, GSH- Px prevents sarcolemma damage and, there­ best biological availability. However, inorganic fore, muscle fiber damage.s selenite is the form most often used for supple­ mentation, since it is least expensive. *Dr. Miller is a 1983 graduate of the College of Veteri­ nary Medicine at Iowa State University. Selenium availability is antagonized by high, **Dr. Thompson is an associate professor in Veterinary nontoxic levels of certain elements in the diet. Clinical Sciences at Iowa State University. These include copper, silver, tellurium, zinc,

96 Iowa State Veterinarian arsenic, and mercury.12,13 Even though this an­ calves. Studies done in England, North Caro­ tagonism has only been shown experimentally, lina, and Ohio indicate that Se/vitamin E sup­ it should be considered when Se-deficiency oc­ plements substantially decreased the incidence curs in heavily supplemented herds. of retained placenta. These cattle were from herds with a history of retained placenta prob­ CLINICAL SIGNS lems and were eventually found to have diets Selenium deficiency affects cattle of all age deficient in Se. 17 ,18,19,20,21 Other recent studies groups. In calves under six months of age, evaluated the effect ofSe/vitamin E supplemen­ three syndromes of myopathy appear, depend­ tation of dry cows on decreasing the incidence ing on which muscle group is affected. of retained placenta; no prevention of inci­ With cardiac involvement, sudden death can dence could be shown. 22,23 Therefore, the role of occur in calves up to two months of age and is Se/vitamin E deficiency in causing retained associated with a period of excitement usually placenta is questionable. precipitated by feeding. On four farms in England, calves exhibited grunting and then died within one minute showing no other CLINICAL PATHOLOGY signs. a All herdmates had low selenium status, A few reliably accurate methods may be and no further deaths occurred after Se supple­ used to determine the Se status of cattle. For mentation. samples of whole blood, tissues, and feed, a If the diaphragm and intercostals are the direct analysis for Se content is widely used. In main muscles involved, the clinical signs simu­ whole blood, normal levels are 0.8-2.5 umol/ late pneumonia. Dyspnea and abdominal liter, and clinical signs occur at levels below 0.4 breathing are observed. umol/liter. 26 For liver and kidney samples, When mainly skeletal muscle is involved, levels of below 3.0 and 30 umol/kg dry matter, lameness, tremors, and symmetrical weakness respectively, indicate Se-deficiency. The liver is are present.15 The muscles of the hind limbs preferred for analysis, since in animals fed Se­ and back are usually involved. In acute cases deficient diets, the kidneys retain Se and there­ the muscles are swollen and hard if palpated. fore give falsely elevated values. 27 For a feed However, in chronic cases they are hard, rub­ sample, a level below 100 ppb is considered Se­ bery and somewhat atrophied. Since muscle in­ deficient.8 volvement is usually generalized, the appear­ Indirect indicators of Se status are glu­ ance of the preceding syndromes can overlap. tathione peroxidase and aspartate aminotrans­ Another syndrome in calves, seemingly un­ ferase enzyme activity, which decrease and in­ related to myopathy, is a Se-responsive unthrif­ crease, respectively, in Se-deficient animals. tiness in dairy and beefcalves. 10 This syndrome GSH-Px levels are probably less affected by the varies from a subclinical growth deficit to a daily diet than blood selenium, since GSH-Px sudden loss of condition, and is commonly as­ is incorporated into erythrocytes during eryth­ sociated with a profuse diarrhea of undeter­ ropoiesis.8 Therefore, GSH-Px might be a mined cause. more constant value and more reliable. Nor­ In yearlings and adult cattle, a nutritional mal values for GSH-Px activity are 3,000 myopathy with myoglobinuria is associated Units/ml of blood or 30 Units/mg of blood. with Se-deficiency. It is more common in year­ Simple, qualitative tests for GSH-Px have been lings and is induced by stress due to transporta­ developed for field use. They are reported to be tion' bad weather, or turning out to pasture in rapid, relatively inexpensive, and able to dif­ the spring.8,16 These factors, in conjunction ferentiate inadequate Se status of cattle. 28,29 with Se-deficiency, likely precipitate the prob­ Two other serum enzymes are used to deter­ lem. The main clinical signs are locomotor dis­ mine muscle damage.The first, creatine phos­ turbance and myoglobinuria. Also in adult cat­ phokinase, is specific for myodegeneration. tle, two reports describe a post-parturient Levels for this enzyme rise quickly to 1,000­ downer cow syndrome resembling milk fever. 16 5,000 mU/ml, but can drop to normal levels in The affected cows were stiff, reluctant to walk, 3-4 days if there is no ongoing myodegenera­ and recumbant in severe cases. tion. With a second enzyme, glutamic ox­ Other problems possibly linked to Se-defi­ aloacetic transaminase, the levels will rise and ciency in cows include higher incidence of re­ drop much slower, but this enzyme is not spe­ tained placenta, abortion, and birth of weak cific for myodegeneration. Overall, the moni-

VOl. 45, .No. 2 97 toring of both these enzymes can indicate if the riodical injections or oral dosing with Se salts, myodegeneration is ongoing or regressing. the use of Se-supplemented salt licks, or possi­ ble addition of selenium to soil to raise the GROSS AND MICROSCOPIC LESIONS forage content. The basic lesion associated with Se-deficien­ For intramuscular, subcutaneous, or oral cy is a hyaline degeneration of striated muscle routes, a dosage of 3-6 mg/100 lbs. B.W. of that is usually more widespread than the gross elemental Se is recommended. 26 This is the so­ lesions indicate. Grossly, whitish-yellow discol­ dium or potassium salt, or selenite or selenate. orations of muscle fibers are vvell defined in In severely deficient areas, treatment may be their long axis, but vary in distribution in the repeated at one to three month intervals, as muscle bundle. These affected fibers are inelas­ necessary. A common treatment regime used in tic, friable, and dry, but may become chalky in studies for retained placenta prevention is 50 texture if calcified. In skeletal muscles the gross mg Se and 680 IU vitamin E intramuscularly lesions show bilateral symmetry and appear in at three to four weeks prepartum. 23 the hind limbs, back, intercostal muscles, and Careful mixing and monitoring of levels in the diaphragn~. feed is necessary if supplementation is at­ Gross lesions in the heart appear anywhere tempted, since toxic levels occur at 30-50 times in the myocardium, but frequently have an an­ the requirement levels. 23 Levels for dry cow ra­ nular distribution around the left ventricle. 15 tion are 0.23-0.92 mg/cow/day during the last Unlike skeletal muscle, the lesion margins are four to eight weeks of gestation. irregular and undefined. Frequently, only a The use of Se-supplemented salt licks and slight pallor appears grossly, while myocardial slow release rumen pellets is frequently necrosis is demonstrated microscopically.14 In described in British literature. Levels recom­ severe cases of acute myocardial degeneration, mended are 2.5- 2.6 mg Se/kg of salt in the salt pulmonary edema, hydropericardium, liver licks and 5 % in the rumen pellets. 31 congestion, and a slight ascites are present. Addition of selenium compounds to pasture In all striated muscle, the histological ap­ or crop land is feasible, but whether it is effi­ pearance is hyalinization with patchy segments cient and cost-effective is questionable. Addi­ of granular and liquefactive necrosis. This is tion to pasture at 30-60 gm/acre is suggested. commonly referred to as "Zenker's necrosis." The protective effect is variable, but may last Also, some fibrosis of the cardiac muscle oc­ years. Since the uptake by plants is variable, curs, which replaces damaged muscle fibers. regular monitoring of feed levels is recom­ mended. DIAGNOSIS Diagnosis is based on clinical, postmortem, REFERENCES and biochemical observations. Differential 1. Combs GF Jr., Noguchi T, Scott ML: Mechanisms diagnoses to be considered in calves are ofAction of Selenium and Vitamin E in Protection of pneumonia, other nutritional deficiencies, and Biological Melnbranes. Fed Proc 34:2090-2095, causes ofsudden death. Se-deficiency should be 1975. 2. Van Vleet JF: Current Knowledge of Se/Vit E Defi­ considered in cows if the herd has high inci­ ciency in Domestic Animals. JAVMA 176:321-325, dence of retained placenta and fertility prob­ 1980. lems, or in heifers if abortion is prevalent and 3. Wood PA, Smith JE: Pathogenesis and Diagnosis of no etiology can be found. Selenium Deficiency. VMISAC 74:206-297, 1979. A presumptive diagnosis is sometimes made 4. Van Vleet JF, Ruth G, Ferrans VJ: Ultrastructural Alterations in Skeletal Muscle ofPigs with S~lenium­ when Se supplementation corrects the prob­ Vitamin E Deficiency. Am J ~t Res 37:911-922, lem, but a definitive diagnosis must be based 1976. on Se levels of blood or liver. 26 It appears, how­ 5. Zingaro RA: How Certain Trace Elements Behave. ever, that GSH-Px activity of blood might re­ ENV Sci Iech 13:282-287, 1979. 6. Sheffy BE, Schultz RD: Influence of Vitamin E and place direct analysis, since it is reliable, quick­ Selenium on Immune Response Mechanisms. Fed er, and more useful in the field. 28,29 Proc 38:2139-2193, 1979. 7. Bayne R, Arthur JF: Alterations of Neutrophil TREATMENT AND PREVENTION Function in Selenium-Deficient Cattle. J Comp Pathol The various manifestations of Se-deficiency 89:151-158, 1979. 8. Chalmers GA, DeCaire M, Zachan CJ, Barnett M: described above can be treated or prevented by Myopathy and Myoglobinuria in Feedlot Cattle. Can supplemental selenium in mineral mixes, pe- ~t.J 20:105-108, 1979.

98 Iowa State Veterinarian 9. Scholz RW, Cook LS, Todhauter DA: Distribution 20. julien WE, Conrad HR, Moxon AL: Selenium and of Selenium-Dependent and Nonselenium-Depend­ Vitamin E and the Incidence of Retained Placenta in ent Glutathione Peroxidase Activity in Tissues of Parturient Dairy Cows. II Prevention. ] Dairy Sci Young Cattle. Am] vet Res 42: 1719-1724, 1981. 59:1960-1962, 1976. 10. National Academy ojSciences-Research Council: Selenium 21. Segerson EC, Rievere Gj, Dalton HL, Whitace in Nutrition. Washington, DC, National Academy MD: Retained Placenta of Holstein Cows Treated of Sciences, 1971. with Selenium and Vitamin E.] Dairy Sci 64:1833­ 11. Carter AH, Scott ML, Noguchi T: Biological Avail­ 1836, 1981. ability of Selenium Compounds for Prevention of 22. Gwaxdauskas FC, Bibb TL, McGilliard ML, et al: Exudative Diathesis in Chicks.] Nutr. 105:96-105, Effect of Prepartum Selenium-Vitamin E Injections 1975. on Time for Placenta to Pass and on Production 12. Wobauger PD, Weswig PH: Influence of 19 Ele­ Functions.] Dairy Sci 62:978-981, 1979. ments on Development of Liver Necrosis in Sele­ 23. Morrow D, Thomas jW, Maw Rj: Effects of Vit E nium and Vitamin E Deficient Rats. Nutr Rep Internat and Selenium on Preparturient Diseases and Fertil­ 18:421-428, 1978. ity in Dairy Cattle. BOD Prac 16:80-81, 1981. 13. Burk RF: Selenium in Nutrition. WId Rec Nutr Diet 24. Hutchinson Lj, Scholz RW, Drake TR: Nutritional 30:88-106, 1978. Myodegeneration in a Group of Chianina Heifers. 14. Cawley GD, Bradley R: Sudden Death in Calves ]AVMA 181 :581-584, 1982. Associated With Acute Myocardial Degeneration 25. Taylor RF, PuIs R, MacDonald KR: Bovine Abor­ and Selenium Deficiency. I:7et Rec 103:239-270, tions Associated with Selenium Deficiency in West­ 1978. ern Canada. Proc Am Assoc I:7et Lab Diag 22:77-84, 15. jubb KVF, Kennedy PC: Pathology oj Domestic Ani­ 1979. mals. Academic Press, 2nd editi~n, 484-488, 1970. 26. Howard JL: Current I:7eterinary Therapy-Food Animal 16. Gitter M, Bradley R, Pepper R: Nutritional Myode­ Practice. W. B. Saunders, p 327, 1981. generation in Dairy Cows. Ti't Rec 103:24-26, 1978. 27. Zingaro F~A, Cooper we: Selenium. 1st E S) P 550, 17. Trinder N, Woodhause CD, Reuton CD: The Effect 1974. of Vitamin E and Selenium on the Incidence of Re­ 28. Berrett S, Herbert CN: A Semi-Quantitative Spot tained Placentae in Dairy Cows. I:7et Rec 85:550-553, Test for Glutathione Peroxidase in Blood of Cattle 1969. and Sheep for Assessment of Biological Selenium 18. Trinden N, Hall Rj, Reuton CD: The Relationship Status. I:7et Rec 105:145-146, 1979. Between the Intake of Selenium and Vitamin E on 29. Backall KA, Scholz R W: Reference Values for a the Incidence of Retained Placentae in Dairy Cows. Field Test to Estimate Inadequate Glutathione I:7et Rec 93:641-643, 1973. Peroxidase Activity and Selenium Status in the 19. julien WE, Conrad HR, jones jE, et al: Selenium Blood of Cattle. Am] I:7et Res 40(5):733-734,1979. and Vitamin E and the Incidence of Retained Pla­ 30. Van Houwling CD: Selenium in Animal Feeds. ]AV­ centa in Parturient Dairy Cows.]Dairy Sci 59:1954­ MA 171 :343-349, 1975. 1959, 1976. 31. Underwood Ej: The Mineral Nutrition of Livestock. Commonwealth Agricultural Bureau) 2ed, p 157, 1981.

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