Why Do Scouring Calves Get So Sick? – Part 3. What happens to the calf during a scours event

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Let us quickly review what we covered in the first two parts of this series. First, there are four main factors in calf scours: dehydration, acidosis, D-lactic acid overload, and endotoxemia. Of these, D-lactic acid overload is the most harmful to the calf.  In a few cases, hypoglycemia or thiamine deficiency may be responsible for abnormal calf behavior. However, hypoglycemia and thiamine deficiency both usually cause rapid, uncontrolled movements, while the toxic effects of D-lactic acid cause depression, lethargy, weakness, and inability to rise or stand, progressing to coma and death. Hypoglycemia and thiamine deficiency will result in death if not corrected, but these conditions are always characterized by rapid, even violent, uncontrolled and uncoordinated movements.  In almost all cases of scours, we will be dealing with the effects of dehydration, acidosis, and D-lactic acid overload.

Scours starts when some disease-causing organism (bacteria, virus, or protozoa) multiplies rapidly in the calf’s small intestine. Many of these species can normally be found in small numbers in the small intestine, and in small numbers they do no harm. However, when they multiply rapidly, they attack the interior lining of the small intestine and damage the lining. The damaged lining cannot absorb nutrients from the milk or milk replacer as efficiently as it does normally. As a result, some partially digested milk flows into the large intestine. Once in the large intestine, the partially digested milk is fermented by bacteria that are normally present in the large intestine. However, when these normal bacteria feed on the partially digested milk, they can produce D-lactic acid, as well as other acids. These acids are absorbed through the wall of the large intestine into the blood stream, and the calf develops acidosis. (Small amounts of L-lactic acid is produced as part of normal body processes. However, L-lactic acid is converted to beneficial products by the liver, and is harmless. However, D-lactic acid is a potent neurotoxin.)

The kidneys will remove L-lactic acid and D-lactic acid from the blood. However, L-lactic acid (which is not toxic in the quantities usually found) is removed much more efficiently than is the D-lactic acid. Once the calf develops acidosis, the kidneys do not work as efficiently, so the D-lactic acid tends to accumulate in the calf’s body. While the undigested milk is being fermented in the large intestine, the damaged small intestine is either (a) not absorbing as much water from the milk as it normally does, and/or (b) water is actually passing from the blood stream into the interior of the small intestine. As a result, the calf’s body does not take in as much water as it did prior to the scours event, and the calf’s body may be losing body fluid into the intestine, further reducing the amount of water in the calf’s body. Either way, the calf begins the process of dehydration. As dehydration progresses, the calf’s kidneys work less efficiently, so the buildup of D-lactic acid is further accelerated. To summarize: the damage to the small intestine directly results in dehydration, and indirectly in the production of D-lactic acid and acidosis. Dehydration and acidosis cause the kidneys to work less efficiently, so the increased production of D-lactic acid occurs just when the kidneys are less able to remove it from the calf’s body. The increasingly severe acidosis causes the calf to not want to eat. The increasing level of D-lactic acid causes the calf to become rapidly weaker. If the D-lactic acid level rises too much, the calf will lapse into a coma and eventually die.

Since many cases of scours are started by viruses or protozoa, antibiotics are not effective. The calf’s own natural defense mechanisms must prevent the organism from spreading further, and lining of the small intestine must heal. These processes do not work effectively when dehydration and acidosis occurs.  Thus, the calf that remains acidotic or dehydrated is less likely to reverse the effects of the initial damage to the lining of the small intestine, and the scours event is more likely to continue until the calf is permanently damaged or dies.

About the Author

Roy Williams
Roy is a retired calf grower, and is now a graduate student in the Molecular and Cellular Biology Program at Dartmouth. He is currently involved in research in the genetic factors of cancer at the Geisel School of Medicine at Dartmouth. His long-range research interests are in parasitism and infectious diseases, particularly in calves.


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