Determining the cause of scours in calves is often difficult. Unlike the majority of monogastric animals, ruminants cannot vomit to expel stomach contents before reaching the small intestine. Newborn calves also make low amount of stomach acid (to protect colostral antibodies), which is a natural inhibitor of viable bacteria entering the small intestine.
Calf scours can be defined as the discharge of more fluid than normal, increased frequency of discharge, and greater loss of water and important electrolytes than is taken in. Normally, considerably more fluid is secreted into and out of the intestine and absorbed than is ingested by the calf. If the normal cycling of body water into and out of the intestinal tract is disrupted, a resulting disturbance of the cycle and risk of dehydration and loss of important electrolytes (salts) can occur.
Two pathways of intestinal fluid disruption can occur during scours:
- Excessive secretion of water into the intestine coupled with normal water reabsorption back out of the intestine
- Normal water secretion into the intestine, but reduced water absorption back into the intestine
The net result of scours is an imbalance of normal body fluids. Dehydration can be evaluated by skin “tents,” a mouth that isn’t slick, limbs and ears are cold, eyes sink and a gap appears between the eyeball and inner lid, urine output drops, and a depression in the attitude of the calf is observed. To evaluate skin tenting, twist a large fold of loose skin in the neck area. A skin “tent” for four seconds or greater indicates moderate dehydration and a need for intervention.
Perhaps one origin of calf scours starts with an upset in the osmolality (concentration of liquids vs. solids) of the intestinal contents. An example would be feeding too great of a concentration of milk solids (not mixing calf milk replacer and water to achieve a total solids ranging from 12.5 to 15%). The higher concentration of milk solids pulls water (through osmotic pressure) from blood and cells into the small intestine. This increased water in the gastrointestinal tract speeds the rate of passage of nutrients through the gastrointestinal tract.
A concurrent disruption in nutrient absorption through the lining of the small intestine occurs as well as a disruption of the normal bacterial flora in the gut. These normal and beneficial bacteria have developed a mutually beneficial symbiotic relationship with the calf intestine and serve to defend the intestine through protection against pathogenic bacteria such as E coli. and salmonella. E. coli have the ability to attach to the intestinal lining, set up shop and reproduce. Irritation of the intestinal lining results in the damage of the enterocytes, which are the cells in the intestine responsible for absorption of nutrients. Once pathogenic bacteria become prevalent in the gastrointestinal tract, they can proliferate in numbers and also increase in their disease-causing ability. Further damage of the small intestinal lining reduces the physical barrier that prevents intestinal contents from directly entering the blood stream.