Grass tetany

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Grass tetany or hypomagnesemic tetany, also known as grass staggers and winter tetany, is a metabolic disease involving magnesium deficiency, which can occur in such ruminant livestock as beef cattle, dairy cattle and sheep,[1] usually after grazing on lush pastures of rapidly growing grass, especially in early spring.

Cow grazing on rapidly grown pasture with tetany of the neck suggesting Grass Tetany

Symptoms and Etiology[edit]

Progressive symptoms may include grazing away from the herd, irritability, muscle twitching, staring, incoordination, staggering, collapse, thrashing, head thrown back, and coma, followed by death. However, clinical signs are not always evident before the animal is found dead.Grass tetany. Kansas State Univ. Research and Extension, Forage Facts series. http://www.ksre.ksu.edu/forage/pubs/97notebook/fora15.pdf

The condition results from hypomagnesemia (low magnesium concentration in blood) which may reflect low magnesium intake, low magnesium absorption, unusually low retention of magnesium, or a combination of these. Commonly, apparent symptoms develop only when hypomagnesemia is accompanied by hypocalcemia (blood Ca below 8 mg/dL).Kahn, M. A. (ed.) 2005. Merck veterinary manual. 9th Ed. Merck & Co., Inc., Whitehouse Station.

Low magnesium intake by grazing ruminants may occur especially with some grass species early in the growing season, due to seasonally low magnesium concentrations in forage dry matter.Rendig, V. V. and D. L. Grunes (eds.) 1979. Grass tetany. ASA Spec. Publ. 35, Am. Soc. Agron., Madison, Wisc. 175 pp. Some conserved forages are also low in magnesium and may be conducive to hypomagnesemia.Mehren, M. Winter tetany and grass tetany http://www.oregonfeed.org/mehren_art_0205.htm

High potassium intake relative to calcium and magnesium intake may induce hypomagnesemia. A K/(Ca+Mg) charge ratio exceeding 2.2 in forages has been commonly considered a risk factor for grass tetany. Potassium fertilizer application to increase forage production may contribute to an increased K/(Ca+Mg) ratio in forage plants, not only by adding potassium to soil, but also by displacing soil-adsorbed calcium and magnesium by ion exchange, contributing to increased susceptibility of calcium and magnesium to leaching loss from the root zone during rainy seasons. In ruminants, high potassium intake results in decreased absorption of magnesium from the digestive tract.Wylie, M. J., J. P. Fontenot and L. W. Greene. 1985. Absorption of magnesium and other macrominerals in sheep infused with potassium in different parts of the digestive tract. J. Anim. Sci. 61: 1219-1229.Schonewille, J. T., A. T. Van't Klooster, H. Wouterse and A. C. Beynen. 1999. Effects of intrinsic potassium in artificially dried grass and supplemental potassium bicarbonate on apparent magnesium absorption in dry cows. J. Dairy Sci. 82: 1824-1830.

Trans-aconitate, which accumulates in some grasses, can be a risk factor for hypomagnesemia in grazing ruminants. (Tetany has been induced in cattle by administration of trans-aconitate and KCl, where the amount of KCl used was, by itself, insufficient to induce tetany.Bohman, V. R., A. L. Lesperance, G. D. Harding and D. L. Grunes. 1969. Induction of experimental tetany in cattle. J. Anim. Sci. 29: 99-102.) Relatively high levels of trans-aconitate have been found in several forage species on rangeland sites conducive to hypomagnesemia.Stout, P.R., J. Brownell and R. J. Burau. 1967. Occurrences of trans-aconitate in range forage species. Agron. J. 59: 21-24. Although at least one rumen organism converts trans-aconitate to acetate,Cook, G. M., J. E. Wells and J. B. Russell 1994. Ability of Acidaminococcus fermentans to oxidize trans-aconitate and decrease the accumulation of tricarballylate, a toxic end product of ruminal fermentation. Appl. Env. Microbiol. 60: 2533-2537. other rumen organisms convert trans-aconitate to tricarballylate, which complexes with magnesium.Russell, J. B. 1985. Enrichment and isolation of rumen bacteria that reduce trans-aconitic acid to tricarballylic acid. Appl. Env. Microbiol. 49: 120-126. Using rats as an animal model, oral admistration of tricarballylate has been shown to reduce an animal's magnesium retention.Schwartz, R., M. Topley and J. B. Russell. 1988. Effect of tricarballylic acid, a nonmetabolizable rumen fermentation product of trans-aconitic acid, on Mg, Ca and Zn utilization of rats. J. Nutr. 118: 183-188. Potassium fertilizer application results in increased concentration of aconitic acid in some grass species.Grunes, D. L., J. W. Huang, F. W. Smith, P. K. Joo and D. A. Hewes. 1992. Potassium effects on minerals and organic acids in three cool-season grasses. J. Plant Nutr. 15: 1007-1025. luke was hear 2013

Epidemiology[edit]

In Northern Europe, the disease occurs after winter housing. But in Australia and New Zealand, where the cows are not housed, the disease occurs in similar conditions, when the animal enters lush, grass-dominant pastures. [2] In North America, grass tetany occurs most commonly when range stock are moved onto lush early pasture or when housed stock are turned out onto such pasture in the spring. A second high-risk period may occur in the fall. Although cereal grasses (e.g. winter wheat) and crested wheatgrass may be especially conducive to grass tetany, the problem can also occur with several other grass species. "Winter tetany" may occur with some silages,[3] low-magnesium grass hays, or corn stover.[4]

Treatment[edit]

The affected animal should be left in the pasture, and not forced to come back to stall because excitation can darken the prognosis, even after adequate treatment.  [5]

Intravenous mixed calcium and magnesium injection are used. Subcutaneous injection of magnesium sulfate (200 ml of 50% solution) is also recommended.[3]

Prevention[edit]

Magnesium supplements are used to prevent the disease when ruminant, for obvious economic reasons, must have access to dangerous pastures.

External links[edit]

References[edit]

  1. ^ Mayland, H. F. 1988. Grass tetany. In: Church, D. C. (ed.). The ruminant animal: digestive physiology and nutrition. Prentice-Hall, Englewood Cliffs, N. J. pp. 511-523.
  2. ^ D.C. Blood, J.A. Henderson, O.M. Radostits (1979). Veterinary Medicine (5th ed.). London: Baillière Tindall. pp. 841–847 (Lactation Tetany). ISBN 0-7020-0718-8. 
  3. ^ a b Kahn, M. A. (ed.) 2005. Merck veterinary manual. 9th Ed. Merck & Co., Inc., Whitehouse Station.
  4. ^ Allison, C. 2003. Controlling grass tetany in livestock. New Mexico State Univ. Coop. Ext. Serv. Guide B-809. http://aces.nmsu.edu/pubs/_b/B-809.pdf
  5. ^ Gustav Rosenberger (1978). Krankheiten des Rindes (2nd ed.). Berlin: Verlag Paul Parey. pp. 1024–1037 (Weidetetanie). ISBN 3-489-61716-9.