VSC 497B Pathology of Nutritional and Metabolic Diseases
Dr. Robert J. Van Saun
A variety of syndromes occur in sheep, goats, and beef and dairy cattle due to a lack of utilizable magnesium (Mg). Nonruminant species are not afflicted by this problem. The symptoms may vary from hyperaesthesia, aggressiveness, incoordination, tetany, and convulsions to flaccid paralysis. Although the pathogenesis of all the hypomagnesemic diseases is probably the same, they are given common names indicating the conditions under which they occur: grass tetany, grass staggers, wheat pasture poisoning, lactation tetany, transport tetany, winter tetany, and milk tetany of calves.
I. Signalment
A. Worldwide distribution of hypomagnesemic conditions, occurring primarily in areas with excellent agronomic practices.
B. Grass tetany, Grass staggers, Lactation tetany (Acute form)
1. Most often older cows (dairy and beef) and ewes in the first two months of lactation, but the disease is by no means confined to this group. Older animals have reduced mobilizable skeletal reserves.
2. It usually occurs in the spring on lush, fast growing grass pastures. Pastures that have been improved by the use of nitrogen and potassium fertilizers are particularly apt to produce the disease. Hypomagnesemia can be seen in the fall when rains stimulate new growth of dry summer pastures. Hypomagnesemia is not commonly seen in alfalfa pastures (may be related to differences in forage sucrose content).
3. Cereal crop pastures. Grazing pastures of wheat, oats, or barley precipitates grass tetany (extremely low magnesium content).
4. Commonly occurs during the first two weeks after animals are turned out from enclosed housing and winter feeds.
C. Transport tetany, Winter tetany, Milk tetany (Chronic form)
1. Winter tetany associated with older pregnant cows being fed on low quality forages (magnesium deficient) during winter time (assuming a spring calving season). Usually coupled with insufficient intake of digestible nutrients.
2. Transport tetany usually associated with feeder and stocker calves which are being shipped long distances after being on poor quality feed. Transport tetany can also be seen in adult cattle being kept off feed with a previous history of poor quality feed being offered. Onset may be associated with the stress of movement.
3. Milk tetany is seen in calves approximately 6 weeks of age, solely on a milk diet. At this time the GI tract becomes less efficient at absorbing magnesium and milk is very low in magnesium.
II. Clinical Signs
A. Acute Tetany
1. Unusual alertness
2. Twitching of the eyes, ears, and skeletal muscle
3. Hyperaesthesia, disturbances may cause attacks of bellowing and frenzied galloping
4. Above signs may lead to recumbency and clonic convulsions with opisthotonos and involuntary nystagmus
5. Body temperature is normal to elevated
6. Acute signs may be precipitated by stress and death may occur within 0.5 to 1 hr if treatment is not instituted.
B. Acute paralysis - in some cases, cattle may develop acute flaccid paralysis, clinically indistinguishable for milk fever.
C. Subacute tetany - same signs of hyperaesthesia, hyperalertness and muscular twitching over a period of 3 to 4 days.
D. Chronic hypomagnesemia - animals with a chronic dietary deficiency may develop signs of poor appetite and unthriftiness. Sudden stress may send them into more acute tetany signs.
III. Pathogenesis
A. Magnesium metabolism - The ruminant animal has limited body stores of magnesium. Daily Mg requirement is > 0.2% of diet dry matter (3-3.5 gm/d Cattle, 1-1.5 gm/d sheep). If the regular dietary supply of magnesium is interrupted, the animal will soon develop a magnesium homeostasis problem. Although there is not much magnesium in milk, this loss usually pushes the situation over the edge with resultant clinical signs.
1. Magnesium absorption occurs primarily in the rumen and reticulum, with some from small intestine
2. Magnesium availability is low 7 to 35%. Dietary availability may be reduced with high potassium rations. Potassium may interfere with the Na/K transport system in rumen epithelium.
3. There is no specific regulatory processes which modulate serum Mg concentrations. Of the total Mg in the body (0.05%), 65-70% is in bone, 15% in muscle, 15% in other soft tissue, and 1% in extracellular fluids. Serum Mg concentration ranges from 1.8 - 2.4 mg/dl (normal) with clinical signs starting below 1.5 mg/dl and severe disease at < 1.0 mg/dl.
4. Daily Mg requirements are a function of age, size, stage of pregnancy, level of lactation, and weather conditions.
B. Biologic Function of Magnesium - Magnesium is a major intracellular cation, which is a metal cofactor for numerous metabolic enzymes including those related to carbohydrate, protein, and lipid metabolism. Extracellular magnesium is responsible for modulating neuromuscular and synaptic membrane potential transmission and bone mineralization.
C. Pathologic lesions due to low Mg
1. reduced Mg intake - dietary deficiency
2. reduced Mg availability - high K diets
3. reduced skeletal Mg mobilization - older animals
4. increased urinary Mg excretion - high Na
E. Predisposing factors for Mg content of forages:
1. rapid plant growth in cool temperatures reduces Mg content
2. heavy rainfall inducing rapid plant growth
3. Nitrogen, Potassium, calcium, ammonia, nitrate, and sulfate fertilization reduce Mg availability to the plant
4. Legumes >>> grasses >> concentrates
5. Forage Mg content < 0.2% may be a potential problem
6. Organic acid content of plants (aconitic, citric, tricarboxylic)
7. Forage scoring system K/(Ca + Mg) if > 2.2 then potential problem
V. Clinical Pathology and Diagnosis
A. Hypomagnesemia
Clinical cases generally have serum magnesium concentrations in the range of <1.0 (chronic) or < 0.5 (acute) mg/dl. Normal values are generally 1.8 - 3.0 mg/dl. Be aware of the normal range for the lab which you are using. Urine Mg concentration of 2.0-10.0 mg/dl are considered inadequate and < 2.0 mg/dl as severe deficiency.
B. Hypocalcemia
Mild to moderate declines in serum calcium concentration (4 to 8 mg/dl) are also seen with hypomagnesemia.
C. Postmortem diagnosis. Difficult diagnosis on necropsy since there are no significant lesions. Serum values of no significance after death as a result of cellular leakage of Mg. Vitreous humor concentrations of Mg have been useful in diagnosing a problem up to 48 hrs after death. Cerebral spinal fluid may also be of benefit.
D. Differential Diagnosis
1. Nervous ketosis
2. Milk fever
3. Lead poisoning
4. Infectious neurological disease - rabies, tetanus, listeriosis
5. Polioencephalomalacia
6. Brain abscess
7. Enterotoxemia (Clostridium perfringens)
8. Nitrate toxicity
VI. Treatment
A. Intravenous infusion of a Ca-Mg solution.
For cattle, 500 ml (50 ml sheep) of a 23% Ca borogluconate solution which also contains 5% Mg hypophosphite (or 15% Mg gluconate). These solutions should be given very slowly (withers high) to prevent cardiac arrest. Serum Mg concentrations will rise rapidly, but return to low levels with 3-6 hrs.
B. Subcutaneous Mg injections.
To prevent relapse, a subcutaneous injection (200 - 300 ml) of a saturated MgSO4 solution (20 - 50%) should be given. This therapy would be insufficient to initially treat without IV injections.
C. Oral supplementation.
After injection of an appropriate Mg solution, clinical cases should receive 50 gm of MgO daily for one week, either as a bolus or mixed in the feed.
D. Enema therapy
An enema of a 30% MgCl2 solution (60 gms in 200 ml water) can be used for initial treatment. Serum and CSF Mg concentrations rise rapidly following enema therapy. This could be a very practical therapy which could be administered by the producer in a period of severe outbreak.
VII. Prevention
A. Animal management techniques - Mg is very unpalatable
1. Dietary supplementation - MgO, MgCO3, MgSO4 mixed in the feed. 8-10 g Mg/d for maintenance, 20-25 g Mg/d for lactating cows; 3 g Mg/d for ewes; 30 g Mg/d for dairy cows.
2. High-Mg mineral blocks or mineral-salt mixes. 1 : 1 : 1 mix of MgO, trace mineral salt and some palatable feed (cottonseed meal, soybean meal, distillers grains)
3. Mg supplementation in single water source
B. Agronomic management techniques
1. Grazing forage having a higher Mg availability
2. Apply moderate amounts of N and K fertilization
3. Apply dolomitic limestone vs. calcitic limestone if liming is needed
4. Use mixed grass-legume pastures when available