Subclinical Acidosis: Is Your Horse At Risk?By Kentucky Equine Research Staff · October 28, 2007
It is no secret among informed horse owners that the horse's gastrointestinal tract is both a wondrous and a delicate creation. When working at full capacity, the tract is able to efficiently convert grasses and grains to energy. When things go awry with the gastrointestinal tract, however, a horse's life might hang in the balance.
Diagrams and descriptions of the equine gastrointestinal tract neatly differentiate the foregut from the hindgut. The foregut includes the mouth and its many components, esophagus, stomach, and small intestine, and accounts for about 35 to 40% of the capacity of the gastrointestinal tract. The hindgut includes the cecum, large colon, small colon, and rectum. The capacities of the foregut and hindgut of the horse are markedly different than those of its barnyard contemporaries. Ruminants such as cattle have significantly more voluminous foreguts that account for 85 to 90% of total gastrointestinal capacity.
Because of the limited size of the horse's foregut, digesta (swallowed food as it undergoes digestion) spends little time there when compared to the hours it spends progressing through the hindgut. One core feature of the hindgut is the fragile population of microorganisms that inhabit it. Anaerobic bacteria, fungi, and protozoa coexist contentedly in the hindgut when the system is working proficiently. Together the microbes' primary responsibility is to digest fiber.
The breakdown of fiber in the hindgut results in the production of volatile fatty acids (VFA), which permeate the walls of the cecum and colon, hitch a ride in the bloodstream, and end up in the liver, where they are used by the horse to fuel athletic or reproductive endeavors.
Causes of Subclinical Acidosis
Certain situations trigger the pH of the hindgut to drop sharply. The two most common causes are the overconsumption of high-starch concentrates or pasture grasses rich in fructan. The demands placed on horses—as athletes and as breeding animals— dictate that substantial quantities of energy-laden feeds be consumed.
When either of these feeding scenarios occurs, it is impossible for the stomach and small intestine to sufficiently digest and absorb the massive onslaught of starch. Accordingly, some starch moves into the hindgut without being adequately digested. As digestion of easily-fermentable starch progresses in the hindgut, the production of VFA and lactic acid increases, causing a significant decrease in the pH. When the hindgut endures insults such as this several times a day, it teeters on becoming overwhelmed with acid. Additionally, because lactic acid is stronger than VFA, it can cause serious damage to the intestinal mucosa. In severe cases, lactate may contribute between 50 and 90% of the total acids in the hindgut.
The shift in pH provides an unfavorable environment for some of the many microorganisms that inhabit the hindgut and aid in digestion. In particular, fiber-digesting bacteria such as Ruminococcus albus and Fibrobacter succinogenes are sensitive to precipitous decreases in pH. For optimal performance, these bacteria favor an environment with a pH between 6.5 and 7.0. When pH drops below 6.0, which is often the case with subclinical acidosis, fiber-digesting bacteria become less efficient and begin to die off.
In contrast to fiber-digesting bacteria, lactate-producing and lactate-utilizing bacteria thrive in an environment with a low pH. Certain microorganisms such as Streptococcus bovis actually shift their metabolism and produce lactic acid rather than VFA when exposed to acidic conditions, serving only to compound the problem.
Changes in the pH of the hindgut due to alterations in the microbial populations and acid profiles cause a condition known as subclinical acidosis.
Signs of Subclinical Acidosis
One of the primary signs of subclinical acidosis is inappetence or decreased appetite. A horse is often reported to be “off his feed.” Because the hindgut is overwhelmed with lactic acid when a horse is experiencing acidosis, the intestinal lining becomes inflamed and irritated, causing the horse discomfort. The irritation may be severe enough to induce behavior characteristic of colic. Furthermore and perhaps most detrimental to equine athletes is a reduction of feed efficiency. Long-term exposure of the intestinal lining to a low-pH environment may negatively affect the absorptive capacities of these structures, limiting the amount of energy available for performance.
In addition to these health concerns, a link between subclinical acidosis and sterotypies such as wood chewing and stall weaving has been suggested by researchers. Because of the precarious nature of the hindgut of a horse afflicted with subclinical acidosis, it is less able to handle metabolic crises that healthy horses may be able to fend off. Therefore, horses with subclinical acidosis are more susceptible to colic and laminitis.