Incidence rates are reported to be between 50 and 100% in performance/race horses with clinical signs including lack of appetite, weight loss/poor body condition, dullness of coat and decreased performance however not all horses with ulceration will show clinical signs of disease. Definitive diagnosis of EGUS currently relies on gastroscopy.
The development of gastric ulceration may be viewed as an imbalance between aggressive and protective factors on the mucosa. Horses continuously secrete gastric acid (even without the presence of feed material in the stomach) and exposure to acid is currently thought to be the major cause of EGUS.
Several nutritional factors have been shown to be associated with the development or severity of gastric ulceration.
It is typical for performance horses to be held off feed prior to exercise for variable times, thus decreasing gastric juice pH, and resulting in more liquid contents. During exercise contraction of the stomach and subsequent “acid splash” may occur leading to acid injury2.
Studies have shown that horses grazing at pasture have a decreased prevalence of EGUS1. During grazing there is a continuous flow of saliva and ingesta that buffers stomach acid, resulting in a stomach pH > 4 for a large portion of the day. When horses are placed in a stabled or yarded environment, they are more likely to have periods of time without access to forage. This leads to a reduction in gastric pH and the nonglandular mucosa is exposed to an acid environment. This intermittent feeding has been reproduced experimentally and shown to produce EGUS.
Concentrate diets are high in hydrolysable carbohydrates which produce large amounts of volatile fatty acids (VFAs) which when broken down can damage the protective barriers of the nonglandular epithelium, allowing hydrochloric acid to irritate and ulcerate the tissue10,11. Several studies have demonstrated a negative effect on the gastric health of horses being fed concentrates as opposed to those on high roughage diets8,1. Horses fed more than 2g/kg bodyweight (BW) of starch per day were likely to have a two-fold increase in gastric ulcer severity score of greater than or equal to 2, compared to eating haylage6. Interestingly, in one study, processing of grain was not found to have a significant effect on the severity of gastric ulceration3.
The size of the meal may also be a factor contributing to gastric ulceration. When horses are fed large, starch-rich meals, intragastric fermentation and VFA fermentation may be favoured because of the large amount of fermentable carbohydrates and the longer retention time within the stomach12.
Repeated oral administration of hypertonic replacement electrolyte solutions has been shown to increase the number and severity of gastric ulcers5.
On initial diagnosis of EGUS, veterinary treatment should be commenced with effective pharmacological agents. Prevention of ulcer recurrence depends primarily on environmental, nutritional and dietary management.
Horses in general should be fed as much fibre/forage as possible2. Pasture turn-out has been suggested to be the best dietary method of controlling gastric ulcers7,13 however some horses and ponies that are very “good doers” may require pasture to be limited, especially those prone to laminitis/metabolic disease. In this situation a lower energy fibre source should be used and if the amount needs to be restricted, the time taken to ingest should be increased (e.g. through the use of slow hay feeders/nibble nets).
Feed hay for fibre. Stabled horses are frequently fed two large feeds a day which results in lower saliva production and increases the rate and extent of intragastric fermentation and gastric emptying rate. The feeding of hay has been shown to increase gastric pH in horses due to the salivary bicarbonate and the buffering effect.
Lucerne hay or a lucerne mix may help to buffer the stomach. One study demonstrated that horses fed a high-protein and high-calcium diet (lucerne based) showed higher stomach pH and fewer and less severe ulcers than horses fed a low protein and high calcium hay diet9. In that study, it was theorised that the calcium in the lucerne hay could have a direct effect on gastric secretions or that the protein was acting as a buffer for the pH. Providing constant access to lucerne hay as part of a balanced diet likely helps to reduce the risk of gastric ulceration. Lucerne has added benefits of being low in non-structural carbohydrate, however it does have a higher energy content compared to some other hay sources which should be factored in when managing bodyweight.
Keep the horse eating. Another effective method used to decrease EGUS is to feed a high-forage diet continuously. The feeding rate for long-stem high quality roughage is recommended at a minimum of 1 – 1.5kg/100kg BW4. Slow feeders/hay nets may be a useful tool to promote ad libitum roughage intake.
Minimise feeding of grain and concentrates. Researchers recommend restricting grain or concentrates to less than 0.5kg/100kg BW every six hours9 and ideally feed < 1g/kg bwt non-structural carbohydrate per meal2. This can be a challenge for some trainers of high intensity exercising horses to achieve without an apparent loss in performance. If additional energy is required, adding fat to the diet of horses will help to maintain energy balance. Added minerals/vitamins may also be required to ensure adequate intake.
It is recommended that electrolyte products be used with caution and may be best given after exercise with feed to minimise their effects on the gastric mucosa12.
A final note on dietary supplements...
There are a plethora of dietary “supplements” or feed additives available on the market claiming to assist in reducing or healing gastric ulceration in horses. These products should be used with caution and only products that have been scientifically tested or have had ingredients that have been shown to have effects on gastric ulcer score in horses should be considered.
Article courtesy of Dr Caroline Foote B.Sc.Agr(Hons). M.App.Sc. Ph.D., Equine Consulting Services Pty Ltd
Is your horse at risk of developing gastric ulcers?