Andy E Durham European Specialist in Equine Medicine, Liphook Equine Hospital, discusses potential strategies for long-term control
We have a reasonable understanding of drug therapy for equine gastric ulcers, but what happens when the course has finished? We must then have a strategy for long-term control wherever possible.
The equine stomach is divided by the margo plicatus into the relatively unspecialised upper squamous mucosa and the lower highly specialised glandular mucosa. Certain areas of the stomach are predisposed to gastric lesions, and, in adult horses, these comprise the squamous mucosa close to the margo plicatus at the lesser and greater curvatures, and also the glandular mucosa in the peri-pyloric region. The commonly affected areas of squamous mucosa are those that are more likely to be exposed to the ventral pool of acidic gastric fluid and thus, squamous mucosal ulcers may straightforwardly be a consequence of acid exposure in this relatively poorly defended region of the stomach. Therefore, risk factors for squamous mucosal ulceration comprise factors that are likely to increase acid contact and injury. In contrast, it is difficult to conceptualise identical risks for peri-pyloric ulcers, which occur in a region that is normally almost constantly exposed to gastric acid, and consequently has evolved numerous defensive mechanisms to
The most logical explanation for the relative weakness of antacid defence in the gastric squamous mucosa is that evolutionary pressures have not been present to lead to its development. Horses evolved as trickle-grazers consuming high-fibre, low non-structural carbohydrate (NSC) grasses over long feeding periods. Observations of the pH and gross appearance of solid ingesta within the ad libitum grass- or forage-fed equine stomach, indicate that the squamous mucosa is normally in contact with bicarbonate-rich-saliva-soaked fibrous matter, which effectively protects this region from acid injury. Voluntary fasting in healthy horses never extends beyond 3–5 hours, and a significant decrease in gastric pH is seen approximately 6 hours after feeding – suggesting the loss of a buffering effect of gastric ingesta (Nadeau et al, 2000). In one study, when less than 0.3 kg hay was consumed over any 4-hour period, the pH in the squamous area was consistently <4, creating significant ulcer risk (Husted et al, 2009). Consistent with these findings, a recent epidemiologic study found that forage feeding intervals greater than six hours represented the strongest dietary risk factor for ulceration of the gastric squamous mucosa Odds Ratio (OR) 5.3, 95% Confidence Interval (CI) 1.4–20, P=0.01) (Luthersson et al, 2009). If long fibre intake becomes restricted then this important protective mechanism will be impaired or eliminated. As the ratio of long fibre to cereal-based concentrate feeds decreases from 100%:0% (as nature intended) towards 30%:70% or even lower, the size and stability of the protective fibrous mass buffer will be reduced, with a more fluid gastric content allowing greater acid exposure and injury, especially in the lowermost squamous regions.
Fast exercise is associated with a decrease in pH of the squamous mucosa, presumably due to acid splashing, and this is significantly mitigated by forage feeding pre-exercise (Lorenzo-Figueras and Merritt, 2002). Given the marked anatomic and physiologic differences between the human and equine gastrointestinal tracts, the anthropomorphic assumption that fast work is best undertaken on an empty stomach is both unfounded and potentially injurious to the equine stomach. Access to forage should be encouraged right up to the onset of fast exercise training, although the argument for weight reduction associated with forage withholding is harder to counter during a competition or race.
Forage quality, quantity and availability, have a significant influence of the likelihood of gastric ulceration. Feeding a diet of alfalfa and grain results in less-severe gastric ulceration than a diet of bromegrass hay or coastal Bermuda grass hay (Nadeau et al, 2000; Lybbert et al, 2007). This suggests a protective effect of alfalfa in comparison to these other forages, possibly via a buffering effect of higher protein and/or calcium content of the alfalfa (Nadeau et al, 2000). A recent study indicated that poor-quality forages were also more ulcerogenic. Horses fed straw were at more than 4 times the risk of having significant squamous mucosal ulcers when compared to those receiving hay or haylage (OR 4.2, 95% CI 1.3–13.8, P=0.02) (Luthersson et al, 2009). In addition to the proposed explanation of calcium and/or protein buffering of gastric acidity, the authors of the latter study also proposed that the highly lignified and silicated nature of straw might be irritating to the gastric mucosa, or perhaps disturb the stability of gastric ingesta stratification.
Associations between cereal feeding and ulceration of the gastric squamous mucosa are well recognised. Coenen (1990) found that 10/27 horses fed a mixed concentrate/hay feed, developed gastric squamous mucosal ulcers compared with 0/21 control horses fed hay only. Andrews and colleagues (2006) proposed that horses fed >0.5 kg grain/100 kg bodyweight every 6–8 hours were likely to be at higher risk for the development of squamous mucosal ulcers. Consistent with this finding, an epidemiologic study found that consuming more than 1 g starch per kg bodyweight per meal (e.g. 1–2 kg concentrates or cereal for a 500 kg horse) more than doubled the risk of having squamous mucosal ulcers (Luthersson et al, 2009). High-cereal diets stimulate a more prolonged gastrin secretory response than forage diets, leading to enhanced acid secretion and even lower pH that might present a greater challenge even to the glandular mucosa. This is also compounded by the reduced salivary buffer secreted in response to rapid cereal meal consumption in contrast to slow and prolonged chewing of forage, and also by slower gastric emptying associated with large, high-starch meals.
Interestingly, despite the relatively poor acid-defence mechanisms within the squamous mucosa described above, studies have shown remarkable resistance to damage when exposed to gastric hydrochloric acid alone (Nadeau et al, 2003a; 2003b). Many weaker, short-chain fatty acids (SCFAs) are generated in the equine stomach from bacterial fermentation of NSCs, including acetic, propionic, butyric, isobutyric, valeric, isovaleric and lactic acids, and these may also be important in fortifying gastric acid and increasing ulcer risk. (Andrews et al, 2006; Nadeau et al, 2003a; 2003b).
Simple acid exposure cannot straightforwardly explain injury to the glandular mucosal peri-pyloric region, which is normally almost constantly exposed to acid and has developed effective mechanisms to protect itself. Indeed, proposed causes of glandular mucosal disease remain speculative. When the equine stomach is continually filled with a physically stable, high-fibre mat of saliva-soaked forage there are beneficial consequences beyond pH buffering and physical protection of the squamous mucosa. The equine pylorus offers little resistance to retrograde flow from the duodenum, and frequent boluses of pancreatic and biliary secretions will enter the stomach unless prevented from doing so by an ever advancing “plug” of fibrous ingesta in a full stomach. The presence of bile acids and also SCFAs produced from duodenal fermentation of NSCs may make bile reflux significantly injurious (Berschneider et al, 1999; Geor, 2000), especially to the peri-pyloric gastric mucosa, which experiences the greatest exposure to duodenal reflux. This theory is supported by this author’s experience of encountering especially severe pyloric ulcers located in the path of duodenal reflux streams.
Furthermore, it may be that physical trauma from ingesta being funnelled into the reduced luminal expanse of the pylorus may serve to remove protective mucus, promoting glandular mucosal injury in this area alone. Bacterial infection of gastric ulcers is common and possibly pathogenically relevant. However, given the abundance of bacteria in the normal equine stomach, it should come as no surprise that bacteria might take advantage of a site where mucosal compromise has occurred for other reasons; therefore, whether or not bacteria have a primary causal role in ulcerogenesis remains to be established.
It is generally accepted that grazing reduces the risks of gastric ulceration in horses, presumably due to similar mechanisms as those described above for forage feeding. However, grazing horses are encountered in practice that have severe squamous mucosal and/or pyloric ulceration. In a study of racehorses, Bell et al (2007) found that the prevalence of gastric ulcers in stabled, partly-grazed and fully-grazed horses was 94%, 89% and 100%, respectively, indicating no protective effect of grazing. Similarly, in another study, a high prevalence of gastric ulcers has been reported in pastured pregnant (67%) and non-pregnant (76%) broodmares (le Jeune et al 2006). This suggests that either other ulcerogenic factors may be capable of overwhelming the protective effect of grazing or perhaps that grazing itself might be ulcerogenic under certain circumstances. The occurrence of severe ulcers in grazing horses is hard to explain, although might result from poor physical stability of gastric content compared with preserved forage. Additionally, as many grasses contain high levels of NSC, this may also serve as a significant source of injurious gastric concentrations of SCFAs that might lead to ulceration as previously described for cereal and concentrate feeds. Studies comparing grass quality and ingestion patterns in grazing horses with and without gastric ulcers might prove interesting in these respects.
Theoretically, beneficial mechanisms of action from dietary oils in high-fat feeds, might include provision of substrate for prostaglandin synthesis (protective for the gastric glandular mucosa), or possibly by binding injurious SCFAs and bile acids within the gastric fluid. Possible increases in gastric emptying rates may also be found in horses fed high-fat versus high-starch diets, thereby potentially limiting SCFA accumulation (Lorenzo-Figueras et al, 2005). Although one study found reduced gastric acid secretion, and higher levels of potentially gastroprotective prostaglandins in horses fed small amounts (45 mL) of corn oil (Cargile et al 2004), a further study that involved feeding higher levels of dietary fat, found no benefit on ulcer severity (Frank et al, 2005).
The equid gastrointestinal tract most likely evolved in association with a diet comprising grasses, rushes and sedges high in fibre and low in NSC, that was gradually ingested in a so-called “trickle-feeding” pattern over perhaps 16 hours each day. It is generally the case that various gastrointestinal dietary intolerances, such as gastric ulceration, are largely explainable in terms of deviations from this natural feeding regimen. It is therefore logical to assume that gastrointestinal health will benefit from attempts to mimic such a diet and ingestive patterns. Indeed, there is evidence that the equine gastrointestinal tract is very poorly adapted to the common practice of feeding cereal and grazing high-quality managed pastures. In practice, it will frequently prove difficult (or impossible) to exactly mimic a natural diet and dietary behaviour owing to the increased nutritional requirements of working horses and the relatively high nutrient density of available feeds, forages and pasture in comparison to the typical feral diet. Nevertheless, potential dietary risk factors can still be identified and moderated in horses that are considered to be at risk of, or found to be suffering from, gastrointestinal diseases.
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(Dietary Control of Gastric Ulcers in Horses first appeared in Equine Health magazine, issue 17, May/June 2014)
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