Grass Tetany

Sodium for the Prevention of Grass Tetany, Bloat, and Fetal Loss in Herbivores Associated with high Potassium and Nitrate, and a Sodium Deficiency.   
  T.W. Swerczek and William C. McCaw
Originally published in BEEF Magazine  June 2012   Reprinted here by permission.

Frosts and freezes to pasture forages in the late Spring provided hints as to the cause of the grass tetany syndrome as well as other syndromes associated with an increase in nitrate and reduced sodium in pasture forages.1,2

Climatic changes involving frosts and freezes seemingly damaged pastures in mid-western and eastern states especially when they occurred in late Spring.  Herbivores, especially horses and cattle, grazing affected pastures often experienced different syndromes related to increased levels of potassium and nitrate.  A correlation existed between the severity of damaged forages due to frosts and freezes and the number of losses in livestock. Our first opportunity to investigate equine fetal losses after late frosts and freezes to pasture forages was in May and June of 1980.3,4  Equine fetuses were affected with several opportunistic bacterial pathogens, which appeared to be secondary to nitrate toxicity.  Fetal tissues and pasture forages revealed high nitrate levels.5  At the same time we also observed other losses occurring in cattle due to grass tetany. 

In late Spring of 2001, another episode of late frosts and freezes happened which also affected pasture forages. During this period, we again observed fetal losses but also detected more cases of grass tetany and acute bloat in cattle. These cows were grazing on pastures with abundant clover. The cattle were dying of acute bloat, consistent with rumen tympany. This type of bloat was not the so-called legume frothy bloat, but was related to gastrointestinal atony.  The pathogenesis of this particular bloat appears similar to the grass tetany syndrome because magnesium and calcium are depleted in the blood due to high nitrate, which disturbs muscular tissues of the gastrointestinal tract.  Magnesium and calcium are critical for muscular tissues, and when a deficiency exists, atony of the gi-tract occurs, causing the gi-tract to become more prone to torsions due to atony and gas formation.6  Local bovine practitioners reported that surfactants, commonly used to prevent legume frothy bloat, seemingly were unsuccessful. We found that cattle did not succumb to acute bloating when adequate loose salt was made available.  A similar finding, in New Zealand,7 was observed in sheep that grazed pastures high in potassium and low in sodium.  We noted that horses and cattle had higher incidences of intestinal problems, which were not related to legume frothy bloat but resulted from torsion of the large intestine.  Animals grazing pastures with adequate sodium were not affected. 7 In 200l, postmortem examinations revealed intestinal displacements and torsion of the large colon, as well as an increase in potassium and nitrate in body tissues. High nitrate was also found in aborted fetuses in 1980 after late Spring frosts and freezes. Additionally, cattle and horses often manifested laminitis.  Furthermore, most herbivores had a dramatic increase in reproductive losses along with a host of secondary opportunistic diseases.   Because of these diseases we suspected a forage induced electrolyte and mineral imbalance.8   The fetal losses and secondary opportunistic diseases were suspected to be due to microbial overgrowth in the gut.9 More importantly, we observed that farms providing adequate salt for animals were having fewer cases of grass tetany, fewer abortions and less death from acute rumen tympany.

A comprehensive review of literature on grass tetany substantiates our findings that sodium is indeed an important factor in the pathogenesis of grass tetany. And, confirms our finding that high levels of potassium and nitrogen in pastures and feedstuffs are likely inducing a sodium deficiency along with a mineral and electrolyte imbalance.

Workers in Holland first noted that intensive managed pastures suppressed sodium in pasture forages that were high in potassium and nitrogen. Cows grazing these pastures showed signs of sodium deficiency.10  Also, Smith and Aines demonstrated that cattle with severe sodium deficiency exhibited clinical signs consistent with grass tetany.11   Workers in New Zealand noted that increased potassium in herbage decreased the uptake of sodium in pasture grasses and legumes.7  After frosts and freezes, potassium increases in pasture forages.  Damaged pastures after frosts and freezes decrease the uptake of sodium.12.  It appears that magnesium is not affected by frosts and freezes.

In the 1950s, researchers in Europe reported that when pasture forages were fertilized with high potassium and nitrogen, there was a dramatic incidence of grass tetany.13  During the same time period, there was great interest in intensive grazing of grass.  Consequently, farmers in Europe heavily fertilized the pastures with potassium and nitrogen. In the Spring, these workers observed a remarkable increase of grass tetany.13   It appeared that when only magnesium was increased in the diet, cattle with grass tetany did not respond.  Interestingly, these workers also considered that cattle may be experiencing a sodium deficiency after pastures were fertilized with potassium and nitrogen.

The British workers decided to treat affected cattle herds with adequate salt, and not with mineral mixes, nor any additional magnesium.   The results were immediate and outstanding because the cases of grass tetany, for the most part, disappeared. Not surprisingly, the same results observed by the British workers 60 year ago were consistent with our findings in affected cattle herds grazing grass pastures with abundant legumes, or pastures recently fertilized with nitrogen. British workers later confirmed that pasture forages fertilized with high potassium and nitrogen did indeed suppress the uptake of sodium.14,15

They also observed an immediate increase in milk production in cattle that were not fed additional magnesium but given adequate sodium.  After recording these results, they recommended to dairymen, whose cattle were affected with grass tetany, to first change their fertilizer program before adding additional magnesium to pastures and to the diet.  Dairymen were also instructed to feed an adequate amount of salt.

Interestingly, British workers did not see an increase in magnesium in the blood of affected animals that were given adequate salt.  A plausible explanation for this is that the high potassium in the diet may have suppressed the absorption of magnesium.  This is a logical hypothesis that has been proposed by Martens and Schweigel.16

However, an additional factor maybe involved.  High nitrate in the diet eliminates excessive magnesium and calcium through the urine and feces and consequently lowers the magnesium and calcium, which becomes unavailable and cannot be absorbed from the gastrointestinal tract as Martens and Schweigel proposed.  Obviously, high nitrate anions in the diet induce a deficiency of magnesium, calcium and sodiumSufficient cations are needed in the diet to counterbalance the excess nitrate anions.  When adequate sodium is in the diet, the surplus nitrate is eliminated through the urine and feces as sodium nitrate.  However, when sodium is deficient, the bi-valent cations are utilized to eliminate the excess nitrate.  Because magnesium is more active it is eliminated first followed by calcium.  When there is an adequate amount of sodium in the diet the excess nitrate is eliminated as sodium nitrate. As a result, the magnesium and calcium are preserved and becomes readily available to be absorbed in the blood.  This hypothesis is proposed in more detail in a report published at growersmineral.com/grass tetany.6 

 European researchers, in previous reports, `advocated that additional magnesium might not be necessary in forages and the diet.  These researchers also suggested that prolonged feeding of high magnesium seemingly reduced milk production.  With our observations in the 1990’s, it appeared that feeding high levels of magnesium over an extended amount of time and also reducing the salt in beef cattle might have caused the wasting syndrome as well as a decrease in milk production.  Likewise, researchers in California reported similar findings in dairy cattle fed excessive amounts of magnesium.  These workers also witnessed a decline in milk production.17

When beef cattle are fed mineral mixes, it is difficult to be assured that all cattle are receiving adequate minerals, including sufficient salt. Often, cattle will refuse to consume these mixes if fed free choice. In some cases, especially related to excessive potassium and nitrate, it may be necessary to force feed the minerals and supply additional salt. Most dairy cattle are fed minerals and salt in complete feed rations. Moreover, it is important that salt, preferably in the loose form, be made available at all times free choice for animals that may desire additional salt.

Clearly, when cattle display signs of nitrate toxicity, from pastures or feedstuffs that are excessive in nitrogen, additional nitrogenous compounds should not be added to mineral mixes that are low in salt, because the low salt entices cattle to eat more nitrogenous compounds. This would be counterproductive.  On the other hand, if diets are low in protein or other nitrogenous compounds, less magnesium, calcium and sodium are necessary in the rations. However, if the protein or the nitrogenous compounds are high, then higher concentrations of calcium, magnesium, sodium and other cations, like iodine, are essential to counteract the excessive anions, primarily nitrate, and other anions, like sulfate, in the diet.

To be more assured that grass tetany, as well as other syndromes do not occur it may be necessary to reduce the dietary potassium and nitrogenous feeds and also provide adequate salt to the ration. These findings suggest that when cattle show signs of grass tetany, milk fever or the downer cow syndrome, they should be treated with magnesium and calcium solutions, and be given sodium in the form of sodium bicarbonate and/or sodium chloride. Previous work has demonstrated that animals with magnesium and calcium deficiency recover when adequate sodium is given.

It is difficult to determine the significance of different levels of nitrate in the blood. When these cations are low in the blood, less nitrate is required to induce toxicity. Conversely, if these cations are high, the same level may be insignificant.  Because nitrate will be affected by the cations in the blood, perhaps, when magnesium and sodium are below normal, nitrate toxicity should be considered as the cause.

Analytical nitrate tests are often problematic and often produce conflicting results. James D. Crutchfield, research specialist in the Department of Plant and Soil Sciences, University of Kentucky, has developed a newly available microplate test for nitrate. The results obtained from the microplate test seemingly are more consistent and reliable.18

References:

1.  Swerczek, T.W. Don’t Short Salt. Beef Magazine, June, 2003. P.14

2.  Martens, H. Outstanding Salt Article. Beef Magazine, August 3. 2003

3.  Swerczek, T.W. Early Abortion in Thoroughbred Mares.  AAEP 26th Annual Convention.  1980;Anaheim, Ca. Nov 29-Dec3

4.   Swerczek, T.W. and Douglas, R.H. Early Fetal Loss and Infectious Placentitis in the Mare.      Third International Symposium on Equine Reproduction.1981; Sydney, Australia. Jan 24-29.

5.  Singer, R. H.:  Livestock Disease Diagnostic Laboratory, University of Kentucky, Lexington, Ky., Diagnostic records, and Personal communications.1980-1981.

6.  Swerczek, T.W.: Nitrate Toxicity, Sodium Deficiency and the Grass Tetany Syndrome. Available at; growersmineral.com/grass tetany. 

7.  Dougherty, C.T., Wells, K.L. and Mitchell, G.E. Sodium in Pasture Species and Grazing Livestock.  Agronomy notes.1995;28(5). Cooperative Extension Service, University of Kentucky, College of Agriculture, Lexington, Ky. 40546.

8.  Swerczek, T.W., Dougherty, C.T., Crutchfield, Dorton, A, and Layton, G.E. ,  MRLS: A forage induced electrolyte and mineral imbalance. K.A.E.P.  Emerging Disease Seminar. March 7, 2002, Lexington, Ky.

9.  Swerczek,T.W. Saprotrophic Fungi and Bacteria and Commensal Bacteria that Infect Frost-Damages Pastures may be Contributing to Gut Microbial Overgrowth and Lesions Associated with the Mare Reproductive Loss Syndrome.  J. of Equine Veterinary Science. 2002;(6) 234-237 

10.  Paterson, R. and Crichton C.H  Grass Staggers in Large Scale Dairying on Grass. Journal of the British Grassland Society. 1960;15:100. and  Fren, A.M.; Physiological aspects of the nutrition of dairy cattle. fifth study meeting Europ. Assoc.. Anim.  Prod.1955; and Personal communications with Frens, A.M.;. by Paterson and Crichton.1957

11.  Smith, S.E. and Aines, P.D. Salt requirements of dairy cows. Cornell Univ. agric. Expt. Sta. 1959; Bull. 938.

12.  Blevins, D.G., M. Remley, K. Lukaszewski, D. Davis. 2011. The loss of sodium in freeze-damaged tall fescue forage could be a major contributor to spring grass tetany.2011; Online. Forage and Grazinglands doi:10.1094/FG-2011-0221-02-RS..

13  Paterson, R. and Crichton  C.H Grass Staggers in Large Scale Dairying on Grass. Journal of the British Grassland Society. 1960;15:100

14.. Butler, E.J. The Mineral Element Content of Spring Pasture in Relation to the Occurrence of    Grass   Tetany and Hypomagnesaemia in Dairy Cows. J. Agric Soc. 1963;60:329.    

15.  Burns, K.N. and Allcroft, R. Hypomagnesaemia Tetany in Cattle. I. Incidence, aetiology, diagnosis and treatment. Br. Vet. J.1967; 123:340-347.             

16  Martens, H. and Schweigel, M.: Pathophysiology of Grass Tetany and  Other Hypomagnesemias. In Veterinary Clinics of North America: Food Animal Practice. 2000;16(2)                                    339-368.

17.  Urdaz, J.H. et. al.  Importance of Appropriate Amounts of Magnesium in Rations for Dairy Cows. Vet Med Today, Timely Topics in Nutrition. JAVMA,2003;222(11)1518-1523.

 18.  Crutchfield JD and Grove JH. A new cadmium reduction device for the microplate determination of nitrate in water, soil, plant tissue, and physiological fluids. J AOAC Int. 2011; 94(6):1896-1905.

 

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