Major metabolic disorders

a. Milk fever This is caused by the heavy calcium demand at the onset of milk production. The cow is unable to meet this demand due to an imbalanced ration. Other factors are inadequate vitamins (esp. vitamin D), poor hormonal response (especially of parathyroid gland), and age (milk fever is seen in older cows, typically after the first lactation). Cows with mild fever stagger, are unable to rise, show muscle weakness, become recumbent and may have a subnormal temperature. If you remember your muscle physiology, calcium plays a key role in muscle contraction. Hypocalcemic cattle lack normal muscle tone (both skeletal muscles, and the smooth muscles involved in swallowing reflexes). Recumbent cattle may develop bloat, which is a major factor in death. Typically signs are seen between 24 hours before and 72 hours after calving. Milk fever predisposes cattle to a host of other problems, particularly slow or difficult calving (due to muscle weakness in uterus and abdominal/pelvic muscles), uterine prolapse, retained placenta, and infections of the uterus (womb). A typical annual incidence of milk fever in herds in the mature cow bunch is around 8%. When the incidence is above this, something is amiss, most often with the diet. It may signify the dietary calcium/phosphorus ratio is out of whack, the diet is too alkaline, or another factor is involved (e.g., incorrect potassium/magnesium ratio). Treatment: Injection with calcium solutions (typically, calciuim borogluconate) is effective . It should be given intravenously when an animal is down. Animals respond remarkably quickly (minutes) and gratifyingly, unless the hypocalcemia is severe and/or prolonged. Oral gels and liquids are increasingly used by producers to treat hypocalcemia in its early stages. This should only be availed of when animals have functional swallowing reflexes.

Control: Ensure normal calcium/phosphorus ratio in diet. The time to do this is a month prior to calving. It is too late for individual animals with milk fever to do this when they are affected. This is done by limiting precalving calcium intake. This may seem counter- intuitive, but the reason is that excess tends to inhibit normal calcium mobilization from the bones. In essence, plenty of calcium pre-calving tends to make the normal endocrine pathway "lazy" and less likely to respond robustly once there is a heavy calcium demand. The diet during this time should be

generally low in calcium. Calcium intake can be excessive when alfalfa, which contains a lot of calcium, is the major or sole component of the diet. Avoid feeding high phosphorus. Keep precalving potassium levels low, since high forage potassium levelspredisposes cows to milk fever regardless of calcium intake. Forages low in potassium are often low in calcium. If this is not practical, consult with a nutritionist about feeding anionic salts to dry cows. Feeding an anionic salt supplement reduces the risk of hypocalcemia as it counteracts metabolic alkalosis, a risk factor for milk fever. The drawback of these supplments is that they can affect the palatability of the ration b. Hypomagnesemic tetany ("grass tetany") This condition occurs in two ways. The classical grass tetany occurs when cattle graze fast growing pastures. We see this in beef cattle in Wyoming. It can affect pastured dairy heifers and dry cows, but rarely in the severe form we see in beef cattle. The pastures may be natural grasses or seeded cereal grains. A typical scenario is a cluser of cases after heavy rains promote lush growth of grass. Signs typically occur within 1 6 weeks of introducing cattle to risky pastures. A second scenario is when housed dairy cows are fed a ration low in magnesium, particularly when the ration is low in energy and high in protein. Often this occurs calving and it can be mistaken for milk fever. Typical signs are restlessness, separation from other cows in the group, hyperreactivity including aggression, incoordination, tetany (stiff legs and neck, particularly when they fall), convulsions and death. Some cattle are found dead. Mild hypomagnesia is more likely to be seen in dairy cattle, often with concurrent milk fever. To help you remember: milk fever = placid cow with flaccid paralysis who just can't get up; tetany = anxious cow over-reacting to environmental stimuli, and may be aggressive to you. One problem: you can see both together. Treatment: Hypomagnesemia is a medical emergency. Magnesium needs to be given intravenously. Crazy-ass maniacal cattle may need to be sedated by a veterinarian first. Some cattle die due to the combination of excitement/stress and hypomagnesemia during treatment. Give the magnesium solutions quietly, with minimal fuss, SLOWLY (over 5 - 10 minutes). It is helpful to give calcium along with magnesium - this helps control cardiac

abnormalities (the heart is a muscle, and the low calcium can trigger fibrillation). Some 80% of treated cattle recover with one treatment. Control: If recurrent on pasture, increase soil/pasture content of magnesium, or administer it as a supplement in the diet or in a molasses lick or to provide additional magnesium to cattle grazing the pastures. As noted above, it is not unusual to see hypocalcemia and hypomagnesia together. Hypomagnesemia blunts the response of the major hormone controlling blood calciium, witht he result both diseases can occur at the same time c. Ketosis Ketosis is a metabolic syndrome where cows are in negative energy balance. It takes its name from the production of ketones, which are water-soluble by-products of fatty acids metabolism. Ketone bodies include acetone, which gives ketotic cattle the its faint but distinctive odor of nail polish remover. In many cases it is easy to recognize because it occurs between the last 2 weeks of pregnancy and first 4 weeks of lactation, typically in a cow in her second to fourth lactation. There is a simple urine test to confirm the presence of excreted ketone bodies - but many producers and veterinarians can smell it off the cow. Ketosis can come with a host of other problems: retained placenta, mastitis, metritis, and displaced abomasum. Ketotic cows should be checked for these complications. Signs include off-feed, weight loss, decreased milk production, listlessness and perculiar neurological signs. In a typical herd it affects about 15% of all early post-partum cows. Treatment: Treatment involves correcting negative energy balance. This can be done by giving dextrose or propylene glycol, or administering corticosteroids. Prevention: Ketosis is prevented by keeping cows in good condition but not too fat during the dry period. Feed changes prior to calving and in the first six weeks of lactation should be gradual. During lactation, a good quality high energy palatable feed should be fed. Owners of herds with >15% incidence of ketosis should consult with a veterinarian or nutritionist for advice on control.