The Texas A&M Veterinary Medical Diagnostic Laboratory (TVMDL) has a rich history. Over the 50 plus years we have existed, TVMDL professionals have worked tirelessly to provide the most accurate and up to date resources to our clients. The following excerpt is part of an ongoing series of articles written by TVMDL’s first director, Dr. William Sippel, and other professionals from the earlier days of TVMDL. Some articles were written for features in The Cattleman publication where others were case studies over recent diagnoses. We hope you enjoy this look back on TVMDL’s history.
Veterinary Outlook: Hypomagnesemia (Wheat pasture poisoning, grass tetany, transit tetany)
By William L. Sippel, V.M.D.
This condition is quite common in Texas from late autumn through the winter to spring. It affects primarily cows 4-7 years old that are nursing calves, but is also seen in nonlactating cattle and rarely in steers or bulls. Sheep are also affected. Low magnesium levels in the blood are noted in this disease but it is not purely a magnesium deficiency.
A high percentage of cases occur in cattle on cereal grain pasture such as wheat, oats, rye or barley, but it is also seen in cattle on grass pastures such as Bermuda. The condition often affects 0.5-2.0% of a herd but can 0ccur in 10-12%.
Weather affects the incidence and inclement weather (“northers”) are usually followed by many cases. A lack of energy feeds in the diet increases the incidence of the condition. Lush growth following rain also seems to increase incidence. Cases appear 1-6 weeks after turning cattle on cereal grain pasture.
Grass tetany is a complex condition, the causes of which are not completely understood. While it is not strictly a magnesium deficiency disease, it can be prevented by feeding “luxury levels” of magnesium (2 ounces magnesium oxide per head per day). An important complicating factor in the wheat poisoning type of disease appears to be the high amount of potassium in wheat pasture. Any small grain pasture well fertilized with potash (potassium) and nitrate is more apt to produce cases than poorly fertilized forage. Apparently the high levels of potassium tie up the magnesium or make it unavailable to the animal. High levels of nitrate possibly raise the rumen ammonia level with similar effects. The fact that grass tetany can follow good fertilization practices places it in the category of good management diseases. In contrast it is seen frequently in animals receiving inadequate amount of energy (poor management), especially following cold weather (or other stress).
Good management and economics dictate that small grain pasture must be fertilized for maximum production, which means providing adequate potassium, nitrate, and phosphorus – all of which may enhance the development of grass tetany. The challenge is to develop a method of inducing cattle to eat enough magnesium while on these pastures. Suggestions listed below.
Clinical signs seen in grass tetany cases are primarily related to the nervous system. Acute cases will chomp the jaws; froth at the mouth; move the ears, eyes, eyelids and facial muscles irractically (sic); stagger; fall; have convulsions; and may die in one of these seizures from respiratory failure. The heart sounds may be very loud and audible a few feet from the animal.
Less severely affected cattle may be restless, have fine tremors of facial muscles; make exaggerated or unsteady movements in walking; have frequent small urinations and defacactions; and may go into a convulsion at the sound of a loud noise. The syndrome may pass and the animal appear normal only to be followed by another episode. Many of these animals become belligerent.
These include lead, insecticide and plant poisonings (such as Dallis grass), rabies, hemophilus infection (“thrombosis”), and other central nervous system diseases. Many cattle affected with the acute form are found dead so the “sudden death” diseases must also be considered. Due to the number of diseases that can be confused with the condition, including rabies and the need for prompt, specific treatment, a veterinarian should be called to differentiate between the possibilities. There are no diagnostic postmortem lesions.
Treatment is the administration of magnesium and calcium salts. This must be done carefully so as not to cause heart stoppage. Consult your veterinarian for advice and/or assistance. The longer treatment is delayed, the poorer are chances for recovery. Prompt treatment is very important.
Prevention is a more difficult and more important aspect. Increasing the magnesium intake in pastured animals should be the goal. It is difficult (and expensive) to induce a cow to consume enough magnesium (2 ounces of magnesium oxide per head per day.) Methods include incorporating it in cottonseed meal (or other concentrate or grain mix), molasses or salt made available to the cattle. Adding magnesium to the fertilizer may work on a few but not on most soils. Feeding legume hay is a good preventative but usually impractical. Magnesium “bullets” for slow release in the rumen have not worked well enough.
A solution in severe problem areas is to utilize the pasture by grazing with animals that are not as prone to the disease such as steers, nonlactating heifers, and cows with older calves.
There is no simple, inexpensive prevention for this problem, so ranchers who expect the disease due to conditions on their place should discuss the problem with their veterinarian or nutritionist and select the most practical solution for their ranch.
Laboratory diagnosis is accomplished in affected cattle by determining the level of magnesium in the blood serum. In dead animals a urine sample can be used to identify magnesium deficient cattle. If neither of the above specimens is available, a few blood samples from cattle in the same pasture will serve to determine if blood serum magnesium levels are dangerously low or normal.