CLINICAL NOTE HYPOCALCEMIC PARESIS IN BEEF COWS IN NORTHEASTERN ALBERTA E. JANZEN'
Herd No. 2: In the fall of 1974, 20 cows were culled from a herd of 120 because of age or condition and placed in a feed yard. They were handfed until they were on ground oats ad lib. The roughage portion of the ration was restricted and consisted entirely of mature oat hay. Two cows developed clinical signs of paresis, depression, hyperaesthesia and tetany two days after one cow was found dead in the pen. Response to routine treatment1 was immediate. The addition of an appropriate amount of a 2:1 calcium phosphorus mineral mix to the ration was calculated and suggested to the owner. Until the results of the blood chemistry analyses were known, the ration was top-dressed with 6 gm of MgSO4 per head per day. The two samples of oats used were found to contain 0.125% magnesium which is considered adequate (8, 14). After the magnesium History and Clinical Findings Herd No. 1: During the winter of 1973-74, analysis, MgSO4 supplementation was discon77 cows were fed mature cereal hay and 10 lbs tinued. In the spring of 1975, one additional ground oats per head per day. A vitamin and case occurred in this group of cows two weeks mineral supplement was offered free choice after additional feed had been prepared withbut consumption was low. The cattle were out the suggested calcium and phosphorus supcorralled and this ration represented the com- plement. Herds No. 3, 4 and 5: In these herds hypoplete diet. Over a period of one month, seven cows developed varying degrees of hyper- calcemia occurred in mature pregnant cows esthesia, tetany, poor locomotion and paresis. sporadically throughout the winter months. These cows were successfully treated (calcium The ration consisted of mature cereal oat hay. borogluconate 93.5 mg, magnesium boroglu- The energy intake was adequate but the vitaconate 32.5 gm) I for hypomagnesemia and min and mineral intakes were inadequate. Rehypocalcemia. Addition of 6 gm of MgSO4 sponse to parenteral calcium therapy was good. per head per day to the ration did not prevent further occurrence of the condition. It was our Laboratory Findings and Discussion The average serum calcium concentration past impression2 that this level of magnesium supplementation was usually effective in pre- of affected cows was 5.6 mg/dl with a range venting further occurrence of hypomagnesemia of 4.2-8.0 mg/dl (Table I). This is similar to when cows were grazing late spring green the average concentration of total serum calcium of 5.21 + 1.36 (S.E.) mg/dl reported grass. for other cases of nonparturient hypocalcemia *Department of Veterinary Clinical Studies, (13). The clinical signs could be attributed to Western College of Veterinary Medicine, Univer- a low serum calcium concentration alone (1, sity of Saskatchewan, Saskatoon, Saskatchewan. 2, 5) or to the low serum magnesium concenPresent address: Veterinary Clinical Centre, Prin- tration, although serum magnesium values of ces Highway, Werribee 3030, Australia. less than 1.0 mg/dl are regarded by some (1, 1Parcal, Pitman Moore Ltd., Don Mills, Ontario. 6) as necessary for severe clinical signs of AlVegreville, Clinic, 2Vegreville Veterinary hypomagnesemia to occur. Observations by berta. 298 1976 vol. no. November, 11, 17, CAN. VET. JOUR.,
Introduction Hypocalcemic paresis unrelated to parturition occurs occasionally in cattle (5, 13). It is believed to be alimentary in origin rather than lactational as in parturient hypocalcemia. Diseases which retard the movement of the intestinal tract, those which decrease transit time, and primary intestinal tract diseases may all cause hypocalcemia (4, 5, 7, 12). Hypocalcemia can also be precipitated by deprivation of feed (1, 5) and by mechanisms associated with estrus (1, 3). Veterinarians in beef cattle practice routinely diagnose and successfully treat hypocalcemia in individual beef cows. The purpose of this article is to record the occurrence of outbreaks of nonparturient hypocalcemia in beef cows.
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others indicate that concurrent with a nonparturient hypocalcemia, hypermagnesemia was observed as often as hypomagnesemia and thus serum magnesium is regarded as a widely varying parameter (13). Clinically early hypocalcemia and subacute hypomagnesemia may be difficult to differentiate, although the treatment response of subacute "grass staggers" is often not as good as uncomplicated hypocalcemia (1). Without an immediate definitive diagnosis specific control recommendations cannot be made. Most cases of hypocalcemia occur in mature cows because the metabolic activity of the bone is reduced and a greater dependence for calcium homeostasis is placed on gut absorption (9, 12). Decreased alimentary absorption could be affected by a relative intestinal stasis (12) or an absolute calcium deficiency in the ration. During the winter months beef cattle are commonly fed on poor quality roughage and the motility of the gastrointestinal tract could be affected by feed quality and a nutritional intake that is influenced by fluctuating weather conditions. Net absorption of calcium from the intestinal tract could be further reduced if inclement weather decreased water consumption (12) or inhibited ergosterol activation in the skin (10). Hypocalcemia arising from an absolute calcium deficiency in daily intake could result from food deprivation (1, 5) or from an inadequate calcium content in the feedstuffs (1, 9). An average for calcium and phosphorus in cereal green feed, similar to that fed cows in northeastern Alberta, was calculated and is shown in Table II. The value reported for calcium is higher than the requirement of 0.15-0.16% as recommended by the National Research Council (14), but lower than the generally recommended value of 0.25% (8). When grain is fed at the levels reported in the histories of Herds Nos. 1 and 2 without adequate consumption of supplemental calcium, daily intake of phosphorus will exceed that of calcium. A borderline calcium deficiency, an upset Ca:P ratio, a vitamin D deficiency and a static alimentary tract could all act in concert to impair calcium absorption and induce clinical hypocalcemia. The condition could occur in a significant number of cows of that herd. The disease can probably be easily minimized by including a quantity of good legume hay in the roughage portion of the ration. If mature cereal hay or crop aftermath must constitute a significant part of the roughage portion of the ration, adequate mineral and vitamin supplementation should be assured either by force feeding with grain or by con299
CANADIAN VETERINARY JOURNAL
TABLE II NUTRIENT COMPOSITION OF CEREAL GREEN FEED ANALYZED AT THE SASKATCHEWAN FEED TESTING LABORATORY, JULY 1972-MAY 1975 (11) Percent
Moisture
Crude Protein
TDN
Calcium
Phosphorus
Average Range
12.93 4-30
7.85 4-13
44.80 36-54
0.18 0.030.50
0.17 0. 300.33
stant surveillance of free choice mineral consumption. Summary Some field observations of nonparturient paresis in beef cows suggest the condition can occur with a relatively high (9-20%) morbidity. The good response to therapy and the cinicopathological findings suggest the basic cause to be a hypocalcemia. Possible factors contributing to the etiology of the condition are discussed. Resume Des observations ciniques relatives 'a une paresie non reliee a la parturition, chez des vaches a bieuf, laissent supposer que cette condition peut survenir avec une morbidite relativement elevee (9-20%). La reussite du traitement et les observations clinico-pathologiques font penser qu'une hypocalcemie serait a l'origine de cette condition. L'auteur commente certains facteurs pr6disposants de cette forme de paresie. Acknowledgments The author wishes to thank Dr. Margaret Haydon for her assistance in accumulating the clinical data, the Edmonton Veterinary Diagnostic Laboratory for the blood chemistry analyses and Dr. 0. M. Radostits for his review of the material. References 1. BLOOD, D. C. and J. A. HENDERSON. Veterinary Medicine, Fourth Edition. London: Bailliere and Tindall. 1974.
2. BOWEN, J. M., D. M. BLACKMON and J. E. HEAVNER. Neuromuscular transmission and hypocalcemic paresis in the cow. Am. J. vet. Res. 31: 831-839. 1970. 3. HESS, A. Two cases of milk fever in cows after oestrus. Can. vet J. 10: 317-318. 1969. 4. HUNGERFORD, T. G. Diseases of Livestock, Eighth Edition. pp. 260-265. Sydney: McGraw-Hill Book Company. 1975. 5. JONSSON, G. and M. G. SIMESEN. Parturient paresis. Aust. vet. J. 49: 252-255. 1973. 6. LUTHMAN, J., J. PERSSON and L. MOLLERBERG. Hypomagnesemia in beef herds. Svensk VetTidn. 25: 600-604. 1973. 7. MARR, A. Hypomagnesemia and hypocalcemia in cattle. Vet. Rec. 70: 945. 1958. 8. MARTIN, J. P. Nutritionist at Alberta's Soil and Feed Testing Laboratory. Personal communication. 1975. 9. MAYER, G. P. A rational basis for the prevention of parturient paresis. Bov. Pract. 6: 2-8. 1971. 10. MAYNARD, L. A. and J. K. LOOSLI. Anima Nutrition. 6th Edition. p. 253. McGraw-Hirl Inc. 1969. 11. MITCHALL, K. G. A Case for Forage Analysis: Twentieth Annual Stockman's Day Report. Extension Division, University of Saskatchewan, Saskatoon. Publication no. 267, p. 60.
1975. 12. MOODIE, E. W. Hypocalcemia and hypomagnesemia. Br. vet. J. 121: 338. 1965. 13. NuRMIo, P., K. RoiNE and P. KoKKIA. Observations on non-parturient hypocalcemia in cattle. Nord. VetMed. 26: 483-491. 1974. 14. NUTRIENT REQUIREMENTS OF DOMESTIC ANIMALS. No. 4, Nutrient Requirements of Beef
Cattle. Fourth Revised Edition. 1970. Washington, D.C.: National Academy of Sciences.
1970.
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