Gastric Ulcer Syndrome
Does one of the horses you know show chronic diarrhoea, colic, poor performance, poor body condition, poor appetite, changes in behaviour or does it stretch more frequently to urinate?
Then it could be that it has the Equine Gastric Ulcer syndrome because those are the clinical syndromes (Andrews 2005).
The Equine Gastric Ulcer Syndrome (EGUS) is a lesion in the mucosa of the horses’ stomach. More precisely, they can occur in the distal esophagus, non-glandular (squamous area) and glandular stomach, and proximal duodenum of horses (Andrews et al. 1999). Most lesions are localized in the non-glandular area of the stomach (Sandin et al. 2000)
The disease develops when protective and inciting factors within the stomach are imbalanced. (Murray et al. 1989; Nappert et al. 1989) Protective factors against gastric ulcers in the stomach environment are: adequate mucosal blood flow, the mucus- bicarbonate layer, mucosal prostaglandin E2, tight intercellular junctions, epidermal growth factor and gastroduodenal motility. Inciting factors are: Hydrochloric acid, Acetylcholine, Bile acids, pepsin. As soon as imbalance occurs it is mainly acid that affects the stomach walls but also pepsin and bile are contributing to the damage of the mucosa. Acid is constantly produced in the parietal cells of the horses’ stomach. Its production is stimulated by histamine, gastrin and acetylcholine. (Chris Sanchez 2004, Murray 2002, Murray et al. 1989, Nappert et al. 1989)
But what does actually cause the imbalance of protective and inciting factors in the stomach.
Causes for EGUS are proven to be exercise, management, stall confinement and transportation. (Murray et al. 2005)
It was found out that horses in hard training do suffer the most from gastric ulcers and that there is a correlation between the level or intensity of training and the prevalence of ulcers. This was proven in a study of Dionne et al. in 2003 where the prevalence and the severity of gastric ulcers in Standardbred horses increased when the intensity of training increased. Moreover, the duration of the training has a negative effect on prevalence and severity of ulcers in racehorse and endurance horses. (Murray 1994, Orsin and Piper 1997)
However, there is a difference regarding the different disciplines. In different studies show horses like jumpers/hunters and dressage horses were affected by ulceration by 58 % - 63%. (Mc Clure et al. 1999; Michell 2001) Nevertheless elite, heavy use western performance horses showed less occurrence of gastric ulcers (40%) (Bertone 2000) and racehorses are affected up to 90% (Murray, 1994) due to the high intensity of training.
Exercise causes the development of gastric ulcers because it does reduce the blood flow of the mucosa (which is probably the most important protective factor of the stomach walls. (Sorbye et al. 1994) It was found increased intra-abdominal pressure while training which resulted in an increased intra-gastric pressure and the displacement of the acid content of the stomach from the glandular to non-glandular section. This causes drop in the pH of the stomach environment causing ulcers. (Murray et al. 2005) Moreover, it was shown that exercise influences gastro intestinal hormones and appetite reduction. (Murray et al. 2005) The latter is therefore also a clinical sign of gastric ulcers.
But horses in hard training are not the only ones being affected by the syndrome. Even leisure horses (used for pleasure, riding lessons or show) were shown to be affected by 37% in the study of Murray et al. (1989). In another study horses were transported to an unknown place and were fed twice daily combined with light training (lunging), another group of the same study was stabled individually and was exercised on an automatic exerciser (15-18 min trot and 10 min walk). They found out that in the short period of 7 days ulcers can develop and thus showed that even in light training horses can get ulcers if they are exposed to management changes (about 70% showed ulcers). (McClure et al. 2005)
The diet plays an important role as well. When we imagine that the horses’ stomach is build for taking in small regular meals of mainly fibrous content it is comprehensible that the restricted stable feeding times do not fit to the natural behaviour of the horse. Diets with high carbohydrates and protein are proven to cause ulcers in horses. (Coenen 1990) The high amount of hydrolyzable carbohydrates in the concentrates are fermented and Volatile Fatty Acids (VFA) are produced which are affecting the non-glandular squamous mucosa (when stomach pH is low) (Nadeau et al. 2003a,b). Grains or other non- fibrous meals are faster absorbed and therewith the stomach is emptied much faster. The acid constantly produced (Campbell–Thomson & Merrit 1987) at the time the stomach is empty does affect the mucosa of the stomach. Moreover, grains can produce increased amounts of gastrin (Smyth et al. 1998) which is as above mentioned one of the main factors producing acid (HCL). Furthermore, it stimulates the production of histamine which is another important factor producing acid (HCL). The high amount of acid which accrues in the stomach causes then the imbalance of protective and inciting factors in the stomach environment. Fibre, however, stays longer in the stomach and absorbs a large amount of the acid in the stomach when it is fermented. (Picavet, 2002)
Alfalfa hay was found to be most likely more protective than other types of forages because of the high buffering properties of high protein and calcium contents. (Nadeau et al. 2000)
Any sort of stress (e.g. transportation) is implicated by an increased cortisol level in the horse. Cortisol causes a reduction in prostaglandin E which is important for the suppression of the production of acid (HCL). Thus, if horses are frequently exposed to stress this might cause gastric ulcers. When looking at the western performance horses mentioned above, which were transported to a minimum of 300 miles in 28 days, it seems doubtful that transport is a major cause for the development of ulcers. On the other hand, there could also be the possibility that sensibility to different factors are breed dependent. In this case would that mean that transport could be a major reason for gastric ulcers in racehorses but not in Quaterhorses. This hypothesis can also be justified when looking at the different prevalence percentages among the different disciplines, the intensity of training is surely one reason but what would happen if a Warmblood would get a similar training schedule as a Standardbred? Would Warmblood horses be affected to the same percentage?
Another point to consider would be that EGUS stays in direct correlation with some common stereotypies. As mentioned above, the stomach of the horse constantly produces gastric acid and to buffer this acid content in the stomach the horse needs its salvia which, however, can only be produced while chewing. In fact, crib-biting and wood chewing are stereotypies performed because of gastric discomfort to actually activate salvia production. This connection between the disease and stereotypies makes the dimension of EGUS quite clear. Clinical syndromes are shown by some horses affected but still there are a lot of horses which were used in studies about EGUS showing no clinical signs although they were affected. So, how many horses showing abnormal/stereotypical behaviour do have in fact EGUS?
When talking about stereotypies we are confronted with a big welfare issue. And surprisingly, I did not read one single article in which this disease was obviously discussed as a consequence of poor welfare of the horse. That is why I want to point out that EGUS is a man-made disease which is caused by inadequate management.
Because how ever you may look at it, altogether the causes for EGUS are all related to management factors – feeding, training and keeping systems.
Andrews FM (2005), “Ulcers in the Stomach and Colon; Diagnosis and Treatment: A Pain in the Gut!” American Association of Equine Practitioners - AAEP -
Focus Meeting, 2005 - Québec, QC, Canada; available from www.ivis.org
Andrew FM, Bernard WV, Byars TD (1999), “Recommendations for the diagnosis and treatment of equine gastric ulcer syndrome (EGUS)”, Equine Vet. Educ.; 1: pp. 122-134
Andrews FM, Buchanan BR, Elliot SB, Clariday NA, Edwards LH (2005), “Gastric ulcers in horses”, J. Anim. Sci.; 83(E. Suppl.): E18–E21
Bertone JJ (2000), “Prevalence of Gastric Ulcers in Elite, Heavy Use Western Performance Horses”, AAEP Proceedings 2000, vol. 46
Campbell-Thomson MC, Merrit AM (1987), “Effect of ranitidine on gastric acid secretion in young male horses”, Am J Vet Res; 48: pp. 1511-1515
Chris Sanchez L (2004), In: Reed SM, Bayly WM., Sellon DC., Equine Internal Medicine 2nd ed. Philadelphia, PA: Saunders Elsevier (USA); pp. 863-873.
Coenen M (1990), “The occurrence of feed-induced stomach ulcers in Horses” Schweiz. Arch. Tierheilkd. 132: pp. 121–126.
Dionne RM, Vrins A, Doucet MY, Paré J (2003) “Gastric ulcers in Standardbred racehorses: prevalence, lesion description, and risk factors”, J. Vet Intern Med.; 17: pp. 218-222
McClure SR, Glickman LT, Glickman NW (1999) “Prevalence of gastric ulcers in show horses”, J Am Vet Med Assoc; 215: pp. 1130–1133.
McClure SR, Murray MJ, Caritheres D, Gross SJ, Hoslste J (2005) “Gastric Ulceration in Horses Exposed to Training and Activities Typical for Recreational Showing”, AAEP Proceedings 2005, vol. 51, Iowa State University
Michell RD (2001), “Prevalence of gastric ulcers in hunter/jumper and dressage horses evaluated for poor performance”, in Proceedings. Annual Meeting of the Association of Equine Sports Medicine 2001; pp. 74-77
Murray MJ (1994), “Gastric ulcers in adult horses”, Comp Cont Educ Pract Vet; 16: pp. 792-794, 797
Murray MJ (2002), In: Smith BP: “Large Animal Internal Medicine” 3rd ed. Philadelphia, PA: Mosby Elsevier; pp. 617-621
Murray MJ, Grodinsky C, Anderson CW, et al. (1989) “Gastric ulcers in horses: a comparison of endoscopic findings in horses with and without clinical signs”, Equine Vet J.; 7 (Suppl): pp. 68-72
Murray MJ, Grodinsky C (1989), “Regional Gastric pH measurements in horses and foals”, Equine Vet Suppl.: pp. 73-76
Murray MJ, Pollmeier MG (2005), “Gastrointestinal Disease and Competition, In: 9e Congrès de Médecine & Chirurgie Equine de Genève / 9. Kongresses für Pferdemedizin & Chirurgie in Genf / 9th Congress on Equine Medicine & Surgery in Geneva, Chuit P. and Montavon S. (Eds.). International Veterinary Information Service, Ithaca NY (www.ivis.org), Last updated: 15-Dec-2005; P1926.1205 [online] (cited May 5th, 2007) Available from: www.ivis.org
Nadeau JA, et al. (2000), “Evaluation of diet as a cause of gastric ulceration in horses” AJVR, 61, 7: pp. 784-790
Nadeau JA, Andrews FM, Patton CS, Argenzio RA, Mathew AG, Saxton AM (2003a), “Effects of hydrochloric, acetic, butyric, and propionic acids on pathogenesis of ulcers in the nonglandular portion of the stomach of horses”, Am. J. Vet. Res. 64: pp. 404–412.
Nadeau JA, Andrews FM, Patton CS, Argenzio RA, Mathew AG, Saxton AM (2003b), “Effects of hydrochloric, valeric and other volatile fatty acids on pathogenesis pathogenesis of ulcers in the nonglandular portion of the stomach of horses”, Am. J. Vet. Res. 64: pp. 413–417.
Nappert G, Vrins A, Larybyere M (1989), “Gastroduodenal ulceration in foals” Compend Cont Educ Pract Vet; 11: pp. 345.
Orsin JA, Pipers FS, (1997), “Endoscopic evaluation of the relationship between training, racing, and gastric ulcers”, Vet Surg 26: pp. 424
Picavet M-Th (2002), “Equine Gastric Ulcer Syndrome”, Proceedings of the First European Equine Nutrition & Health Congress, Feb. 9, 2002 – Antwerp Zoo,
Belgium. [online] (cited May 8th, 2007) Available from: www.ivis.org
Sandin A, Skindell J, Haggstorm J, Nilsson G (2000), “Post mortem findings of gastric ulcers in Swedish horses older than age one year: a restrospective study of 3715 horses”, (1924-1996), Equine Vet J. 32: pp. 36-42
Smyth GB, Young DW, Hammond LS (1998), “Effects of diet and feeding of post-prandial serum gastrin and insulin concentrations in adult horses”, Equine Vet J. Suppl 7: pp. 56-59
Sorbye H, Svanes K (1994),
“The role in blood flow in gastric mucosal defense, damage
and healing”, Digest Dis; 12: pp. 305-317
Use of the terms "Ultimate Horse Site", "The Ultimate Horse Site", "Ultimate Horse", "UltimateHorse", "The Ultimate Horse" have been in use since 2000 and use of variations of our name for any reason is prohibited.