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Equine Gastric Ulcer Syndrome (EGUS): Causes And How To Prevent It

Equine Gastric Ulcer Syndrome (EGUS): Causes And How To Prevent It

The equine stomach consists of an upper non-glandular or “squamous” area (food enters into this part from the oesophagus) and a lower glandular region, which are divided by a line in the stomach wall called the margo plicatus. Gastric ulcers can occur in both areas and the umbrella term “Equine Gastric Ulcer Syndrome” (EGUS) is used as a description. However, recently this has been refined into two separate descriptions based on the location of the ulcers in the stomach wall: Equine Squamous Gastric Ulcer Syndrome (ESGUS) and Equine Glandular Gastric Ulcer Syndrome (EGGUS).

The lower glandular region produces acid on a continuous basis which means the glandular part of the stomach has a pH of approximately 3.0 however, it also secretes mucus and sodium bicarbonate to form a mucosal barrier which protects the wall against this acid. Thus, when EGGUS occurs it is due to a failure in this normal defence mechanism, but the exact cause of this type of ulceration is still unknown with theories that potential contributing factors include bacterial infections (similar to human gastric ulceration caused by Helicobacter pylori), non-steroidal anti-inflammatory medication and stress.[vc_single_image image=”21904″ img_size=”full”]Normally, roughage in the diet will form a large bolus in the stomach which then acts as a buffer to stomach acid and this maintains the upper/squamous part of the stomach at a neutral pH of 7 under normal conditions. The upper squamous part of the stomach does not have the same mucosal defensive system against stomach acid as the lower glandular region.

As horses are placed into training regimes the prevalence of ESGUS, the more common form of ulceration, increases and several management factors has been shown to increase the risk of ESGUS some examples of which include high grain/low roughage diets, increased exercise causing increased intra-abdominal pressure which pushes gastric acid up onto the squamous lining, and full-time stabling. Poor performance has been associated with the presence of ESGUS in both Thoroughbred and Standardbred racehorses.

Diagnosis And Prevelance

The only definitive method for diagnosis of the presence of gastric ulceration is through a fasting gastroscopy with the use of a 3-metre endoscope, which is passed through the oesophagus into the stomach of a sedated horse. This allows for visualisation of the internal wall of the stomach and thus any ulcers or lesions present can be classified based by both location and severity. Different clinical scoring systems for grading the severity of gastric ulcers exist. Diagnosis by treatment is also used.

However, this will not confirm the presence or absence of ulcers in the stomach wall and, generally, only ESGUS responds to the standard treatment. Other methods of diagnosis such as faecal occult blood and sucrose permeability testing have not been proven reliable.

The reported prevalence of EGGUS (risk factors not well described to date) is lower than ESGUS. ESGUS prevalence increases with increasing intensity in work. The highest values reported to date have been for horses in training with a prevalence in Thoroughbred racehorses of over 90% in some studies, elite endurance horses with ulcers identified in 93% of individuals in competition, and 87% of Standardbred racehorses affected in one study.

Obviously, the prevalence values observed will depend on many variables some of which include (but are not exclusive to) the horses being in or out training, breed of horses, nature of training and competition and type of study performed. However, even taking into account that low-grade ulcers are also counted in such prevalence calculations, it is clear to see that gastric ulcers are a health issue for many types of competition horses and potentially can have a negative impact on performance.

Management And Medical Treatment

Management adjustments can have an important contribution to the healing of ulcers. These changes have a higher impact when treating ESGUS than EGGUS due to the differences in the pathophysiology of both syndromes as described above. Management changes include dietary adaptations some examples of which include increased roughage, incorporation of some of this roughage as straw, reduction in the amount of Non-Structural Carbohydrate (NSC) in the concentrate diet and increased oils/fats in the diet.

Dietary modification additionally has some merit for use in EGGUS as the diet has been shown to be a risk factor for this form of the disease as well. Other management changes can include increased turnout time, free access to fresh water at all times and changing feeding time to be within an hour of exercise.

Although management changes may be beneficial in preventing ulcer development, pharmaceutical intervention may be required for established ulcers to achieve full healing, so that the appetite of the horse returns fully. The mainstay for medical treatment of these gastric ulcer conditions is to reduce the amount of hydrochloric acid which the parietal cells in the stomach release in response to histamine binding to H2 receptors, acetylcholine binding to M3 receptors and gastrin binding to gastrin receptors.

There are two classes of drugs used to do this: Proton pump inhibitors and H2-receptor antagonists. Proton pump inhibitors block the release of the gastric acid from the parietal cells by irreversibly blocking the H+ K+ ATPase proton pump which secretes the acid into the stomach. New pumps must then be made before acid secretion can continue and this means these drugs are given once per day. The most common proton pump inhibitor used is omeprazole.

There are different forms of this drug on the market for horses some of which are gastro-protected to increase bioavailability. It must be stated at this stage that the healing rate of ulcers using this treatment after 4 to 5 weeks is approximately 80% for ESGUS but only 25% for EGGUS. This is due to the difference in the causes of the two types of ulcer.

H2-receptor antagonist work by competitively blocking histamine binding to the H2 receptor on the parietal cell and thus their efficacy will depend on maintaining high plasma concentrations. They have a similar structure to histamine and so are selective for H2 receptors. Cimetidine and Ranitidine are two examples of this class of drug with Ranitidine being four times more potent and having more scientific proof of effectiveness. These drugs are usually used in cases where proton pump inhibitors are ineffective in some horses due to poor absorption.

Antimicrobial therapy is used in some cases of EGGUS. However, the routine use of these for EGGUS is not recommended due to the fact that bacterial infection has not been conclusively shown to be a cause of these types of ulcer and there are no clinical trials published to prove the efficacy of antimicrobials in EGGUS.


Nutraceuticals are appealing to use in the case of gastric ulcers as they are easy to use and readily available. Some of the medical treatments can be quite expensive, especially omeprazole. Even though omeprazole has been shown to reduce ulcers if used prophylactically this may come at some cost to the owner. Therefore, oral nutraceuticals have a role to play in the prevention or reduction in the onset and severity of gastric ulcers either in high-risk groups, or animals which have been previously treated for ulcers (in an attempt to prevent reoccurrence of these ulcers).

Mucosal protectants such as sucralfate and pectin-lecithin complexes can be used in an attempt to form a physical barrier on the surface of the ulcer lesions and can be used to relieve the symptoms of ESGUS and EGGUS however variable results on their positive effects for the treatment of ulcers have been reported in the scientific literature to date. Sucralfate forms a thick gel in a very acidic environment and adheres to the mucosal lining of the stomach and ulcer lesions for up to 6 hours. It also promotes the production of new mucus as part of the mucosal barrier.

Calcified seaweed has been reported to have a positive effect on buffering of pH in cattle rumens and equine stomachs and also observed to reduce ulcer lesion severity in horses. Plusvital Neutragast contains a good supply of calcified seaweed in the form of Lithothamnium Calcareum. This will act as a buffer against excess acid within the stomach.

The product additionally contains Boswellia extract which contains several compounds (Terepenes and Boswellic acids) which have been shown to have several beneficial effects which include anti-inflammatory properties, analgesic properties and increased speed of healing from infections. Boswellia compounds have been shown to have beneficial effects in cases of intestinal inflammation and this is achieved through modulation of the inflammatory cell (leukocyte) response. These compounds within the extract have also been reported to inhibit ulcer production in rats.

Plusvital Neutragast additionally contains 1 gram per dose of the amino acid Threonine which is one of the main amino acid components of the protein mucin. Mucin forms a gel-like structure which makes up the mucosal barrier which protects the stomach wall against its own acidic secretions.

Finally, Plusvital Neutragast contains probiotic Saccharomyces cerevisiae (active yeast) which promotes intestinal health through multiple pathways including increased fibre digestion. The formulation of targeted ingredients in Plusvital Neutragast makes it a good nutraceutical candidate for use as an adjunctive management strategy, which can be used in addition to the medical treatments outlined above or additionally post-medical treatment for gastric ulcers to aid in reducing the re-occurrence of ulcer lesions.[vc_btn title=”Learn more about Plusvital’s Support range of supplements here” style=”3d” shape=”square” color=”blue” size=”lg” link=”|||”]

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Designed to neutralise lactic acid during episodes of tying-up and act as a buffer when acidosis occurs.