Why Do Scouring Calves Get So Sick? – Part 2. Continuing introduction to scours, and related abnormal conditions
In the first installment of this series, we discussed four important factors in calf scours: dehydration, acidosis, D-lactic acidosis, and toxemia.
The relationship of dehydration, acidosis, D-lactic acid over-load, and toxemia is complex. Dehydration and acidosis are mostly the result of different processes in the body, and they do not necessarily occur together. Most calf growers have experienced the occasional calf that scours badly, and whose eyes are dramatically sunk back in their sockets, yet the calf appears to act normal and even eats an almost normal amount of milk and water. These rare calves somehow become dehydrated so quickly, and by mechanisms that are not completely understood, that they are not significantly acidotic, and do not have significant amounts of D-lactic acid in their systems. Many more calves develop what is known as “acidosis without dehydration”. Calves that develop “acidosis without dehydration” do not appear (and really are not) dehydrated. These calves will often be over a week old, and may have just gone through a scours event. In most cases, calves that are acidotic will not be willingly taking their full ration of milk, or they eat very slowly.
We have learned that neither dehydration alone, nor acidosis alone, causes the weakness, depression, inability to stand, coma, and death that is characteristic of severe scours cases. These symptoms are caused by a buildup of D-lactic acid. In most severe cases, the excessive D-lactic acid contributes significantly to the overall condition of acidosis. However, we can treat the calf for the acidosis and we will not relieve the D-lactic acid overload and the effects of the D-lactic acid on the calf’s nervous system (and thus its effect on the calf’s behavior). These perhaps surprising relationships have been demonstrated with some elegant experiments that were published between 1999 and 2005, primarily by I. Lorenz in Germany and J. Naylor in Canada.
Before continuing our discussion of these different factors in calf scours, we should mention two other conditions that can cause highly abnormal behavior in calves: hypoglycemia, and thiamine deficiency. Hypoglycemia may be present in calves that are cold stressed and are fed an inadequate ration. An inexpensive hand-held blood glucose meter used in human medicine for diabetic care will yield proper data for calf care. Blood glucose levels under 60 will indicate hypoglycemia; levels over 120 are commonly seen in very ill calves or calves that are undergoing severe environmental stress or injury. In calves that can still suck from a bottle, 100 to 200 cc of 50% dextrose solution given orally is usually sufficient to restore somewhat normal behavior in calves that test positive for low blood glucose levels. A calf that exhibits violent uncontrolled muscle contractions (rapid mouth movements, shaking, rapid eye movements, and intermittent uncontrolled kicking) that does not have an abnormally low blood glucose level may have a thiamin deficiency. Thiamine deficiency can arise following a prolonged episode of scours. Thiamine deficiency is best corrected by administration of 50 to 100 mg of thiamine. In properly fed calves, both hypoglycemia and thiamine deficiency are rare. If you have more than a very rare instance of hypoglycemia (as indicated by the blood glucose meter), you should change your calf feeding program to provide more nutrition to your calves. If you find that calves that have been scouring for several days are becoming hypoglycemic, you should change your scour treatment protocols (as will be discussed in a future installment of this series). It should be noted that the hypoglycemic effects of a marginal feeding program will become most apparent after a sudden drop in the temperature of the calf's environment. Calves who are hypoglycemic will also exhibit low body temperature, but low body temperature alone is not sufficient to diagnose hypoglycemia.