Salt Can Prevent And Treat Grass Tetany

Research by a veterinary pathologist indicates salt is a big factor in preventing and treating grass tetany.Without adequate sodium in the blood, the body grabs onto the most available cation, which would be magnesium, followed by calcium.When the cow consumes frost-damaged forage and the spike of nitrate occurs, her body accesses magnesium in the blood to eliminate the nitrate. This depletes the body and the cow goes down.

Heather Smith Thomas

March 27, 2012

11 Min Read
Salt Can Prevent And Treat Grass Tetany

Editor’s note: Thomas Swerczek does not, nor did the article “The Grass Tetany Puzzle” intend to, espouse the elimination of trace mineral supplements in grazing programs. Rather, the point of the article was that salt has been overlooked as a potential prevention and treatment factor in grass tetany. It is a condition that, in the U.S., occurs mostly in eastern areas where cattle have access to cool-season grasses.We apologize if there was a lack of clarity on this point.

Grass tetany goes by many names – grass staggers, milk tetany, wheat pasture poisoning, and barley poisoning, to name a few. Just as varied as its name has been the speculation as to the cause of this condition. Grass tetany affects mature cattle that graze lush forage following the freezing of early-spring pastures or the sudden growth after rainfall following a drought. The condition mostly occurs in the eastern U.S. in areas with cool-season grasses.

Thomas Swerczek, a veterinary pathologist in Kentucky, thinks the answer may be sodium deficiency.

Grass tetany was first described in Britain in 1930, and was associated with magnesium deficiency and a coexisting calcium deficiency, as well as excess potassium in the blood of affected animals. During cool, wet conditions or regrowth after frost or drought, sodium levels in certain forages plummet, while nitrogen and potassium levels spike.

The traditional recommended preventive has been supplemental dietary magnesium, with treatment consisting of oral and/or intravenous magnesium. But, after examining cattle lost in 2001 following spring frosts in the Midwest – and then analyzing the pastures – Swerczek uncovered some clues about the cause and prevention of grass tetany.

“When I came to Kentucky in 1969, the common preventive for grass tetany was to feed more magnesium. But, cattle wouldn’t eat magnesium free-choice due to its bitter taste, so it was mixed with other feed. And, some farmers fed meat and bone meal, which is high in magnesium,” Swerczek says.

Then, the feeding of dicalcium phosphate and inorganic minerals became common. “Animal scientists and nutritionists thought some forages were poor quality and we needed to add minerals for better utilization. But such supplements still didn’t prevent grass tetany syndrome,” he says.

So, producers evolved to supplementing magnesium during the 2-3 weeks of lush spring growth. When that didn’t reduce grass tetany incidence, Swerczek says nutritionists recommended initiating supplementation even earlier – 4-5 weeks before peak pasture growth.

“That didn’t work, either. So they recommended starting in February, before the grass starts growing. By the 1980s, the recommendation was year-round supplementation, to get it into the animals’ bones,” Swerczek explains. The idea was cattle would access the magnesium out of bone storage when blood levels dropped due to sudden pasture changes.

A change in condition

Swerczek’s training includes veterinary medicine and comparative and nutritional pathology. As a pathologist, he did diagnostics and necropsies on livestock until the early 1970s. Then, he worked as an equine diagnostic research pathologist for 15 years.

In 1986, his necropsy research moved to all classes of livestock. Upon resuming necropsies on cattle, he was shocked to see how much worse the grass tetany situation had become during his hiatus.

“The dead cattle were arriving in a wasted condition I hadn’t seen before 1971, when I’d stopped doing cattle necropsies.” Then, in 1995, he began to see cattle with adult salmonellosis, coccidiosis and other calfhood diseases, which didn’t make sense.

Some pathologists observing the poor condition of cattle coming in for necropsy thought producers weren’t feeding enough protein, Swerczek says. “But when grass tetany problems peaked in 1995-96, the purebred breeders were hit the hardest. So, I began evaluating mineral mixes and visiting some of these purebred herds.”

Swerczek collaborated on this project with William McCaw, a DVM searching for answers in several purebred herds. McCaw also had surmised that something related to diet was causing wasting and opportunistic diseases, he says.

McCaw and Swerczek convinced a handful of producers to stop feeding high-mineral, low-salt mixes in order to serve as a control in their observations. When Swerczek started looking at herds throughout the state, he found a Hereford-Simmental crossbred herd whose owner was feeding loose salt rather than the conventional high-mineral, low-salt mix. (This herd was healthy and did not show any signs of wasting like the cattle on surrounding farms.)

“He still used salt houses – little run-in sheds with a feedbunk for loose salt, to keep it out of the weather. Most farmers had moved from loose salt to mineral mixes and salt/mineral blocks,” Swerczek says.

But this rancher had a salt house in every pasture, and wasn’t supplementing magnesium. “He’d been in the cattle business more than 40 years and never had a case of grass tetany,” Swerczek recalls. Was this an indicator that perhaps supplemental magnesium wasn’t needed to prevent grass tetany?

Later, several herds that stopped feeding the high-mineral, low- salt mixes quickly started to turn around. “Most of the cows had diarrhea and were wasting away. But, within 24-48 hours of giving them loose salt, the cattle improved,” Swerczek says.

In particular, Swerczek recalls working with a 1,000-head Angus herd at that time. Driving across the farm with its manager, Swerczek says they encountered a cow that had been down for several days despite multiple treatments with magnesium and calcium. Swerczek had some sea salt, and put it in front of the cow.

“The manager went back three hours later and that cow had gotten up and wandered off. She went down again, however, so he put more salt in front of her. He went out the next morning and she’d gotten up and rejoined the herd,” Swerczek recalls.

Elsewhere in the herd, other cattle were showing signs of grass tetany and going down. “I told the manager to put a handful of salt in front of them or get it into their mouths to see what happened; they all came out of it. So, I asked if he’d be willing to take away high-mineral, low-salt mixes and replace it with high-salt, trace-mineral mixes. He agreed to try it with a small group confined in a separate pasture. The next cold spell, the cows with access to high-salt, trace-mineral mixes were unaffected by tetany, while the other cattle were affected.”

 In the late 1990s, Swerczek says he visited a farm where cattle were dying in one pasture but not another. The owners had purchased 800 yearlings and pastured half on a farm they owned, with the rest on an adjacent rented farm. On their farm, which featured fertilized clover, the cattle died the following spring, but there were no deaths on the rented pasture across the fence.

“In analyzing the pasture, I found high nitrate and extremely high potassium in the fertilized plants. At first, I thought the problem was related to potassium; later, experiments showed it was a combination of potassium and nitrate.”

Why does salt work?

Swerczek reasoned that cows go down with grass tetany due to a deficiency in magnesium and calcium, but he didn’t know why salt worked. He then used horses as a research model because similar nitrate-toxicity symptoms were seen in horses when grazing frost-damaged pasture.

Swerczek began by feeding some horses extra protein to raise protein and nitrogen levels in their blood.

“I knew nitrate was involved so I measured nitrate in their blood and put some of the horses on salt, and some on no salt. I found that without salt, the nitrate spikes. When horses had an adequate amount of salt, blood nitrate went down to very low levels,” he explains.

“We’d been taught for many years that nitrate isn’t toxic; it’s only toxic if converted to nitrite. However, nitrate in excess may be indirectly toxic if it interferes with the magnesium and calcium metabolism,” he says.

The animal’s body must eliminate excess nitrate and does this through the cations, especially sodium, he adds.

“Without adequate sodium in the blood, the body grabs onto the most available cation, which would be magnesium, followed by calcium,” Swerczek explains. When the cow consumes frost-damaged forage and the spike of nitrate occurs, her body accesses magnesium in the blood to eliminate the nitrate. This depletes the body and the cow goes down.

“If there’s enough salt available, the body can grab onto the sodium and cows won’t go down with grass tetany. But, if you don’t have salt out on the day this hits, they go down. It must be there all the time, and it can’t be hard salt blocks because cattle can’t eat enough when they suddenly need it,” Swerczek says.

Another piece of the puzzle fell into place after Swerczek learned that some farms – despite having adequate salt out – were losing cattle; the cattle weren’t eating enough of it. The potassium level in grass was spiking after a hard frost, especially when it was lush and highly fertilized. Potassium was 15 times more than normal.

“Since the cations, potassium and sodium, are so close together, the body can’t always differentiate between them. People sometimes use ‘lite’ salt (half potassium chloride, half sodium chloride) to reduce sodium intake. These minerals can substitute for one another. When pastures are high in potassium, if there is nitrate in the damaged grass, they come up together as potassium nitrate,” he explains.

Swerczek theorized that when potassium spikes, even though cattle have salt available, they won’t eat it because the body thinks they already have enough sodium. The animals are actually sodium-starved. but their bodies can’t differentiate between excess potassium and too little sodium.

The body has the ability to keep sodium levels within normal range, but when it gets below that, you only have a few hours before that animal dies. “If you feed excess salt, however, and the animals eat it, they’ll be fine – as long as they have plenty of water,” he explains.

Findings confirmed

“British scientists in the 1930s noticed salt could prevent grass tetany, but no one put it all together. Grass tetany should be called nitrate toxicity/salt deficiency leading to hypomagnesia/hypocalcemia,” Swerczek says.

As grass tetany tends to occur in the eastern half of the U.S., due to the predominance of cool-season grasses, Swerczek contacted Dale Blevins, a professor of plant science at the University of Missouri, to discuss his theory.

Blevins says he first became aware of sodium’s role in grass tetany during a cow/calf/tetany study performed with graduate student T. Ryan Lock. Lock published two refereed journal articles on phosphorus/magnesium/tetany in 2004 in the journal Forage and Grazinglands as a result of his study. During his thorough review of the literature, Blevins says Lock also found several refereed journal articles from England/New Zealand, many on lactating ewes, where a relationship between sodium and tetany was being studied.

Swerczek encouraged Blevins to research the relationship between adequate sodium in the diet and how it prevents grass tetany. When a catastrophic weather episode occurred in spring 2007, with warm weather followed by frost, Blevins analyzed fast-growing tall fescue to see what changes occurred during frost. He published an article in the February 2011 edition of Plant Management Network linking salt deficiency and grass tetany.

Analysis of the grass revealed that sodium had plummeted, but there was no change in magnesium. Blevins says the outbreak of grass tetany in April 2007 wasn’t due to low dietary magnesium, but impaired magnesium absorption. Since magnesium absorption from the rumen is dependent upon sodium, the sodium deficiency (due to freeze injury and drying of young fescue leaves) could be the most damaging consequence of a spring freeze.

“Blevins confirmed what I’d been telling cattlemen for over 10 years – they should use adequate salt in the diet to help prevent grass tetany,” Swerczek says. Blevins also recommends now that, to reduce the risk of grass tetany following spring frosts and freezes, sodium supplementation should not be overlooked for grazing animals.

Swerczek is convinced that excess potassium and nitrate causes an acute depletion of magnesium and calcium in the blood if there is a deficiency of sodium in the blood. His detailed paper on nitrate toxicity and sodium deficiency is available here.

Sidebar: Salt isn't foolproof

Thomas Swerczek, a veterinary pathologist, cautions that free-choice loose salt isn’t a foolproof preventive of grass tetany, because cattle won’t always consume enough salt if there is excess potassium and nitrate in the diet or forages.

“It may be necessary to force-feed salt (including it in the daily feed ration) or use a salt-mineral mix very high in salt and low in other minerals. It may be necessary to add something to ensure cattle consume some each day,” he says.

Swerczek recommends a pure product like sugar, or adding the salt to a grain ration to entice cattle to consume more sodium when cattle are at risk for grass tetany.

“Stockmen must be careful that salt-mineral mixes don’t contain excessive trace minerals or toxic heavy metals. Excess salt can be eliminated by consuming adequate drinking water, but excess trace minerals or toxic metals can’t be neutralized or eliminated by drinking water,” he says.

Heather Smith Thomas is a rancher and freelance writer based in Salmon, ID.

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