Nitrate Toxicity, Sodium Deficiency and the Grass Tetany Syndrome
By T.W. Swerczek, DVM, Ph.D.
The clinical signs of grass tetany and milk fever are often similar, and probably the triggering mechanisms are also similar. Without exception, most researchers have observed that clinical signs of grass tetany rarely occur unless affected animals are high producing and being fed a ration high, or excessive, in protein which includes non-protein nitrogenous compounds.
In his 1930 scientific report, Sjollema states that grass staggers (tetany) occurs most frequently during springs in which there is a superabundance of young, rank, quick-growing grasses rich in proteins and during the winter when feed is excessive in protein. Some cattle exhibited disorders suggesting some necessary ingredients were lacking, and he also found the sodium-content in the blood was subject to fluctuations. It is likely the cattle were experiencing a sodium deficiency.
In the 1950s Smith and Aines experimentally deprived sodium from dairy cows and induced clinical signs of grass tetany. Paterson and Crichton discovered low concentrations of sodium were found in tetany-prone grass and prevented grass tetany with sodium chloride. In a field study, Butler observed an increased incidence of grass tetany with low sodium concentrations in the grass and its incidence disappeared at sodium concentrations above 0.2%.
Unfortunately, this early grass tetany work demonstrating the importance of adequate sodium has been either overlooked or ignored, as the majority of today's mineral supplements are deficient in sodium and excessive in magnesium. This is causing weight loss, wasting, severe diarrhea, and reduced milk production when fed with high protein rations. Urdas, et. al. reported on the importance of appropriate amounts of magnesium in rations for dairy cows, especially in rations high in protein, as excessive magnesium had drastic adverse effects on milk production and other clinical signs, including diarrhea.
The clinical signs of grass tetany and milk fever are often similar, and probably the triggering mechanisms are also similar. Without exception, most researchers have observed that clinical signs of grass tetany rarely occur unless affected animals are high producing and being fed a ration high, or excessive, in protein which includes non-protein nitrogenous compounds.
Martens and Schweigel work relating to grass tetany suggests excessive NH+ may interfere with the absorption of magnesium from the gut, as does the lack of sodium and excessive potassium. Numerous researchers have found that grass tetany occurs most often in older brood cows grazing in early spring lush growth. Analyses of these affected pastures during and after frost and freezes revealed elevated levels of potassium and nitrate.
Since sodium aids in the prevention of hypomagnesemia and hypocalcemia, in high producing cows on high nitrogenous rations, it was suspected immune suppression, reproductive losses and other opportunistic diseases in horses, are likely related to nitrate increases in their diets. To test this hypothesis, horses were given a high protein diet with and without the addition of sodium and the levels of nitrate in the blood were analyzed. Diets without the addition of sodium saw marked elevation of nitrate in the blood, whereas, the supplementation of sodium chloride, or zeolytes high in sodium, to the same high protein ration returned the nitrate levels in the blood to normal levels within 24 hours. These findings suggest that sodium indeed is neutralizing the nitrate in the blood, and/ or gut by and is likely being eliminated by the kidneys, in the feces, or in the milk in lactating animals. The high nitrate in the milk may also explain why neonates seemingly are affected with a multitude of opportunistic gastrointestinal diseases, including gastric ulcers and other intestinal disorders. Conversely, dams fed a low protein diet and adequate sodium rarely have neonates suffering from these gastrointestinal disorders.
When there is a deficiency of calcium and sodium and excessive potassium and nitrogen in the soil, it is likely there will be a dramatic spike in potassium and nitrate in pasture forages during and after frosts and freezes. If these affected forages are consumed, they may induce toxicities and/or mineral and electrolyte imbalances. Nitrate in the diet is utilized. However, if it is excessive it may be converted to nitrite by the gut bacteria and methemoglobinemia could occur.
Adequate levels of sodium in the body and ration will lessen or prevent the drastic effects of nitrate toxicity, and it will lessen or prevent grass tetany associated with high potassium and low magnesium levels.
Most cattlemen assume they have adequate sodium if cattle have hard salt blocks, but the most dominate animals in a herd will horde a salt block and the rest will leave without any salt during periods of acute needs. Even the animals that horde the hard block cannot consume enough salt. It is imperative to either have adequate sodium in the complete rations, which is preferable, and/ or to have it always readily available in the loose form, especially when there are nitrate spikes in forages. It is important to place salt mixtures near fresh water sources.
The livestock feed industry has limited sodium chloride in supplements to encourage the consumption of more minerals, and this has led to the over consumption of essential minerals normally not toxic. Sodium restriction is seemingly contributing to hypomagnesemia, hypocalcemia, the downer cow syndrome and a host of opportunistic diseases and may be resulting in decreased performance, especially in dairy cow milk production and severe reduction in weights of calves on beef cows.
The forced feeding and overfeeding minerals, often contaminated with heavy metals, has drastic effects. It is important to have adequate, high quality, pure forms of calcium and magnesium in the diet of high producing animals. Adequate access to sodium also appears to help alleviate acute deficiencies during spikes in nitrate.
Some cattlemen, either intentionally or unintentionally, allow cattle to go without salt, sometimes to allow the easily gathering of salt starved cattle. If there is a spike in potassium and nitrate due to adverse environmental conditions while deprived of salt, cattle are often found dead. Seemingly, cattlemen with the healthiest cattle are very aware of the need for cattle to have unlimited access to loose salt and/ or loose trace mineralized salt at all times.
The nitrate anion per se is relatively non toxic in cattle and horses, unless it is excessive and converted to nitrite by bacteria in the gastrointestinal tract. But indirectly it appears to be inducing mineral, electrolyte and ionic imbalances, and secondary immune suppression. Sodium chloride, sodium bicarbonate, and high sodium zeolite compounds appear to neutralize the toxic effects of excessive nitrogenous diets.
Nitrate toxicity is difficult to evaluate. It is imperative to consider nitrate levels in forages and well as in the blood of affected animals. Nitrate levels in the blood and biological fluids are difficult to interpret as the amount and the duration of exposure need to be considered. Excessive nitrate in the blood is eliminated by excretion and can give the false impression that nitrate toxicity did not occur as it may have been previously excreted not be apparent when analyzed.
Cattle and horses with apparent nitrate toxicity, and cattle with clinical signs of grass tetany, will have elevated levels of aldosterone. Aldosterone is a steroid hormone produced by the adrenal gland and acts to conserve sodium and secrete potassium, and increase blood pressure. Elevated aldosterone levels indicates that the system is attempting to conserve sodium, which is deficient, and substituting potassium, which is excessive, for sodium. Aaldosterone levels, therefore, may be the best indicator of ionic imbalances induced by the excessive nitrate anion.
In summary, hypomagnesemia and hypocalcemia are more likely to occur in high producing animals that are fed diets high or excessive in carbohydrates and proteins, including non-protein nitrogenous compounds, and nitrate. When this happens, it causes a "washing out" effect of essential cations including calcium, magnesium and sodium in the urine, feces and milk, thus hypocalcemia, hypomagnesemia and hyponatremia. A simple prophylaxis is not to overfeed protein and carbohydrates to herbivores, but this is not always practical when striving for maximum production. However, it can be somewhat alleviated by feeding adequate calcium, magnesium and sodium, preferably in complete rations, but also they should be available free choice. Calcium and sodium if fed at optimum concentrations are non toxic, but magnesium if fed at high levels for prolonged periods, may be toxic and may result in chronic wasting, reduced milk production and diarrhea. Seemingly, the feeding of adequate levels of magnesium and increased levels of calcium and sodium during period of environmental stress will prevent grass tetany.
The article has been shortened considerably from the original which was presented at the Annual Growers Nutritional Minerals Meeting, Milan, Ohio, December, 2007. The complete text with cited references is available from the Growers office. Dr. Swerczek's address is 664 Providence Road, Lexington, KY. 40502.
