Modern feeding practices have increased the risk of colic in our horses. Here’s why.
Colic: it’s an ever-present threat for domestic horses. As an owner, if you haven’t had to do battle with it yourself, you certainly know someone who has – and you likely know someone who has lost a horse to colic, as well.
The problem is that many cases of colic stem directly from the way we manage our horses: not for their digestive health and happiness, but for our own convenience.
The horse evolved as a wandering, grazing animal, consuming forages high in structural carbohydrates, almost around the clock. His gastrointestinal system does the majority of its processing of these carbohydrates through fermentation in the cecum (part of the large intestine), with the help of beneficial bacterial populations that reside there. The end result of this fermentation is Volatile Fatty Acids (VFAs), which are absorbed across the gut wall and supply nutrition and energy to the horse’s cells.
The digestive picture changes, however, when grain becomes part of the horse’s diet. Grain is necessary to help supply the extra energy needed by a performance horse, but it has a downside, especially when it is fed in large quantities.
Under normal circumstances, the concentrated starches and sugars contained in grain are processed in the small intestine. But the digestive tract is designed to constantly move food along its length ... so when a horse is fed a large grain meal, some of it may pass undigested from the small intestine on to the next stage, the fermentation vat of the cecum. The results of grain reaching the hind-gut are well-documented: the sugars and starches are fermented by the hind-gut bacteria, a process which produces lactic acid. As the pH of the environment inside the cecum drops with the heightened acid production, the mucosal lining is compromised, and hind-gut acidosis sets in.
Meanwhile, the bacteria that normally ferment forage begin to die off in the increasingly acidic environment, to be replaced with pathogenic bacteria. This “bacterial inversion” can lead to a cascade of endotoxins in the horse’s system. The combination of lowered pH, bacterial inversion, and a buildup of toxins can lead to the formation of colonic ulcers (ulcers in the colon).
COLONIC ULCERS: MISSING PIECE OF THE COLIC PUZZLE?
It’s not hard to imagine that a hind-gut whose surface is pitted with colonic ulcers might function abnormally. Evidence that hind-gut acidosis and resulting ulceration can compromise motility, digestive efficiency, and blood flow to the digestive tract, is mounting.
In one study sponsored by the Japan Racing Association, the anterior mesenteric artery (AMA), which runs from the heart along the right dorsal colon, and feeds the last few feet of the ileum (the lower portion of the small intestine) was injected with endotoxins produced by dying bacteria. It induced symptoms of colic in the study horses within 20 minutes.
We can surmise that a horse with bleeding colonic ulcers experiences reduced blood flow to his digestive tract through two avenues: constriction of the blood vessels due to loss of pressure, as well as the influx of endotoxins. There are several peer-reviewed studies which support this:
- Julliand et al., in 2001, showed that rapid fermentation of starches in the hind-gut alters the microbial ecology. Specifically, they found that Lactobacillus and Streptococcus bacteria proliferate, creating an accumulation of lactic acid and other organic acids in the cecum.
- Clark et al, in 1990, found that an unbalanced microbial population associated with the production of lactic acid in the hind-gut causes two problems: first, a decrease in pH that depresses fiber digestion and, second, an increase in the potential of certain microbes to release endotoxins.
- Swyers et al, showed in 2008 that disturbances in the pH of the hind-gut can predispose horses to endotoxemia and laminitis.
- Weiss et al. demonstrated in 2000 that exposure of colonic mucosa to cecal contents incubated with starches, resulted in increased permeability of the colon walls, which could allow endotoxins to quickly enter the bloodstream.
Colonic ulcers have not been studied to the same extent as gastric (stomach) ulcers, largely because of the difficulty of detecting them in a living patient. Unlike gastric ulcers, they cannot be examined with an endoscope; yet necropsy results on hundreds of horses indicate that colonic ulcers are at least as widespread as gastric ulcers. In studies over five years, on a total of 750 equine carcasses, we found an incidence of physical signs of gastric ulcers ranging from 43% to 60%, and of colonic ulcers ranging from 44% to a shocking 87%.
Many of the early warning signs of colic, such as intermittent diarrhea and sensitivity along the flanks (especially the right side, where the cecum empties into the right dorsal colon), might also be warning signs of colonic ulcers. Other preliminary signals which could alert an owner to a possible colonic ulcer problem include:
- girthiness (a tight girth squeezes on the cranial portion of the colon)
- difficulty or resistance to bending and collection
- grain in the manure, which can indicate that the horse is attempting to process starches in the hind-gut instead of the stomach and small intestine
TREATMENT OF GASTRIC ULCERS A CONCERN
Another concern, and possible contributing factor to colonic ulcers, are gastric acid-inhibiting drugs such as ranitidine, cimetidine and omeprazole, which have become popular in the treatment of gastric ulcers. Suppressing the production of stomach acids on an ongoing basis can leave the horse less able to process grains in the stomach and that will inevitably send poorly digested starches on to the hind-gut, initiating or exacerbating hind-gut acidosis and eventual colic.
In the process of examining over 1,500 equine cadavers, we also noted the unusually flaccid nature of colons having low pH. Could the poor muscle tone of these colons predispose a horse to torsion colic (aka ‘twisted gut’)? There is no proven link at this time, but it bears thinking about.
Most of us can agree that intermittent feeding of concentrated grain meals, along with relatively low levels of forage, is likely to continue to be the norm for most horses. If one were to read and follow recommendations of an equine veterinary manual from 100 years ago, things would be radically different and, perhaps for the horse, so much better.
Franklin L. Pellegrini, DVM, is Vice President, Veterinary Medicine at Freedom Health LLC
Julliand V. et al. Feeding and microbial disorders in horses: Part 3—Effects of three hay:grain ratios on microbial profile and activities, J Equine Vet Sci 2001;21(11):543-546.
Swyers KL et al. Effects of direct-fed microbial supplementation on digestibility and fermentation end-products in horses fed low- and high-starch concentrates, J Anim Sci 2008;86:2596-2608.
Clarke LL et al. Feeding and digestive problems in horses: physiologic responses to a concentrated meal. Vet Clin North Am Equine Pract 1990;43(8):433-450.
Weiss DJ et al. In vitro evaluation of intraluminal factors that may alter intestinal permeability in ponies with carbohydrate-induced laminitis. Am J Vet Res 2000;61(8):858-861.
Oikawa et al. Equine endotoxemia: pathomorphological aspects of endotoxin-induced damage in equine mesenteric arteries, J Vet Med 2002;A-49:173-176.
Oikawa et al. Arterionecrosis of the equine mesentery in naturally occurring endotoxemia. J Comp Path 2004;130:75-79.
Oikawa et al. Mesenteric arterionecrosis in natural and experimental equine endotoxemia. J Comp Path 2006;134:47-55.
Pellegrini FL, Results of a large-scale necroscopic study of equine colonic ulcers, J Equine Vet Sci 2005;25(3):113-117.
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