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January 19-21, 2018
FAEP 55th Annual Ocala Equine Conference

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Gastric Ulcers: A Pain in the Gut!

September 2012

by Frank M. Andrews, DVM, MS, DACVIM

Gastric ulcers are common in horses, with a prevalence estimated from 53 to 93%.1-3 Gastric ulcers can lead to decreased performance, vague clinical signs and may go undiagnosed for months. Gastric ulcers are primarily caused by stomach acids. However, the anatomy of the stomach, diet, restricted feed intake, exercise, stress (stall or transport), and the use of non-steroidal anti-inflammatory agents (NSAIDs) are risk factors for development of gastric ulcers. Because many factors are involved in the cause of gastric ulcers, the term Equine Gastric Ulcer Syndrome (EGUS) was coined in 1999 to describe the condition of erosions and ulcerations occurring in the distal esophagus, non-glandular (NG) and glandular stomach, and proximal duodenum of horses.4 All ages and breeds of horses are susceptible to gastric ulcers and current therapeutic strategies focus on blocking gastric acid secretion and raising stomach pH. Pharmacologic agents are needed to treat these conditions, however, a comprehensive approach including correcting the underlying cause, environmental management, and dietary manipulation is needed for successful prevention.

PATHOGENESIS - Horses are continuous hydrochloric acid (HCL) secretors, and acid exposure is the primary cause of NG gastric ulcers in horses. Also, performance horses are typically fed low-roughage, high grain diets containing water-soluble carbohydrates (WSCs). A diet high in WSCs provides substrates for gastric fermentation by resident bacteria. Gastric fermentation by-products, such as volatile fatty acids (VFAs), alcohol, and lactic acid (LA), may damage the NG squamous mucosa. Several species of bacteria (Lactobacillus, Streptococcus, E. coli) were isolated from the stomach of horses, adding credence to this theory.5 Previously, an in vivo study in cannulated horses showed that a diet high in WSCs and protein (alfalfa hay/sweet-feed grain diet) produced high VFA concentrations in the stomach.6 The presence of VFAs (butyric, propionic, and valeric acids), carbohydrate fermentation by-products, and low gastric juice pH were important predictors of ulcer severity. Furthermore, these VFAs have been shown to disrupt chloride-dependent Na transport within the NG mucosa and cause cell swelling and ulceration.7,8 HCl (gastric juice pH < 4.0) acts synergistically with VFAs on the NG mucosa to cause further damage.

Glandular ulcers are likely caused by a breakdown in the protective factors, such as reduced blood flow, decrease in prostaglandins, and decreased mucus secretion. Stress and the use of NSAIDs are important in causing ulcers in this region.

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