In swine, gastric ulceration refers to the destruction of part(s) or all of the pars esophagea (non-glandular stomach) with the formation of single or multiple bleeding ulcers.
The lesions occur in pigs from weaning onwards; the prevalence is variable but high (5-90%) in most swine-producing areas. Clinical signs are usually only noticed in pigs eight weeks of age or older, with highest prevalence in pigs 120 pounds to market weight. Ulcers occur in all breeds, both sexes and in most major swine-raising countries.
Ulceration of the pars esophagea (UPE) was first reported in Illinois in 1897. Subsequently, the lesion was identified in at least 30 other countries. Although the ulcers most often are subclinical, death losses have been severe enough that much research has been directed at identifying cause(s) and risk factors.
The etiology is unknown but is likely multifactorial and represents the culmination of various permutations of any of multiple risk factors. Risk factors are largely empirical, discerned at the time animals experience higher incidence of the disease. Recently, inconsistent feed consumption associated with respiratory disease outbreaks and/or hot weather seems to be of greatest concern. Other risk factors commonly mentioned include:
- The feeding of finely ground feed (< 400 µm particle size).
- Pelleted rations, perhaps because of the finely ground feed used in making pellets.
- Concentrated, nutrient dense diets that are low in fiber.
- Stress factors (e.g. anxiety, fear, pain, fatigue, crowding, fasting, prolonged transportation, social stress from mixing with unfamiliar pigs, poor air quality, etc.) are frequently suggested.
- Greater occurrence in hot, summer months may be related to inconsistent feeding behavior or stress associated with access to water.
- Out of feed events. This may be a result of inconsistent feed availability from plugged or empty feeding systems or be the result of disease-induced anorexia.
- Greater occurrence reported in barrows (versus gilts) and in high-lean genotypes.
- Feeding rations with copper as a growth promoter, perhaps without adequate zinc.
- Ad libitum feeding of cheese whey or skimmed milk has resulted in increased prevalence.
- Diets high in wheat or cornstarch, compared to barley or milo, and/or low in protein.
- High levels of unsaturated fats in the diet, often with inadequate vitamin E.
Infectious organisms and use of non-steroidal anti-inflammatory agents and the presence of Helicobacter pylori are associated with human gastric ulcers that occur in glandular portions of fundus and pylorus. When pigs have been used as models for human ulcers, ulcers are induced in glandular mucosa. However, naturally occurring ulcers in pigs are in the non-glandular pars esophagea. A primary infectious etiology has not been proven nor is likely for swine. Several agents have been associated with increased prevalence and severity of UPE, including other Helicobacter spp or Gastrospirillum spp, but a causal role has never been established. In some severe “outbreaks” of gastric ulcers in swine, porcine circovirus type 2 (PCV2) has been demonstrated within lesions. Gastric ulceration is a common sequel to outbreaks of swine influenza and porcine respiratory disease complex (PRDC), particularly during summer months.
Both etiology and epidemiology are speculative. Epidemiology is difficult to assess. Risk factors that appear important in one herd or production system do not remain consistently important across others.
Irrespective of cause or risk factors, the effects are thought to be a derangement of normal gastric function. An abnormal fluid content in the stomach results in changes in the pH gradient that normally exists between the terminal esophagus and the pylorus. This results in an excessive, gastrin-stimulated acid secretion. The excessive acidity, lower than is normal at the pars esophagea, initiates changes in the stratified squamous epithelium (hyperkeratosis) that may ultimately lead to ulceration. Pre-ulcerative hyperkeratosis is extremely common in growing swine, probably because of high concentrate/low fiber diets. The pars esophagea undergoes hyperkeratosis and parakeratosis which develop fissures that expose the underlying lamina propria. If the insulting acidity persists, or animals become anorexic, part or all of the stratified squamous epithelium peels or sloughs off and leaves one or more ulcers. Blood vessels of various sizes in the lamina propria are eroded and hemorrhage begins. If blood loss is slow, melena, generalized pallor, and anemia may be observed. If a few large vessels are eroded, the animal may die from an acute massive hemorrhage. In some pigs, the ulcers may be recovered with epithelium and heal uneventfully. Occasionally, resolution of lesions results in stricture of the terminal esophagus or pars esophagea.
Pre-ulcerative hyperkeratosis of the pars esophagea is common as a precursor to actual ulceration. Hyperkeratosis does not appear to influence feed consumption nor is it noticeable clinically. In fact, most swine are subclinically affected, evidenced by the high prevalence of lesions in apparently normal pigs at slaughter. Withholding feed will cause some pre-ulcerative lesions to erode in a relatively short time, as little as two to three days.
Clinical effects of ulcers are usually related to blood loss. Acutely affected pigs may be found dead with pallor. Others may have black tarry feces (melena), anemia, and generalized pallor. Other signs that sometimes can be observed include anorexia, grinding of the teeth, or unthriftiness.
Pigs that die suddenly have pallor of the skin and internal organs and tissues. There may be large blood clots in the stomach and/or blood mixed with ingesta, throughout the intestine. The intestinal, and/or colonic contents are often very dark, black, or “tar-like.” The entire pars esophagea may be eroded to muscular wall giving the false impression of intact glandular mucosa.
Ulcers typical of UPE occur only in the non-glandular region (pars esophagea) of the stomach at the junction of stomach and esophagus. Pigs that are in the early stage of developing ulcers have an altered pars esophagea which, instead of being snowy white, is raised, roughened, somewhat nodular, usually bile stained, and sometimes fissured with hyperkeratosis. Ulcers vary greatly in size, shape, number and depth. Large ulcers often are deep and have smooth, rolled and raised borders. Sometimes the ulcerated area involves the entire pars esophagea and may partially obstruct the esophagus. The terminal part of the esophagus may also be hypertrophied. In animals that have recovered from deep ulcers, a puckered or stellate scar often remains. Complete destruction of the pars esophagea is easy to miss at necropsy; the color of that area may be a uniform gray and without hemorrhage. The absence of clotted blood in the stomach does not rule out UPE; careful examination of the pars esophagea is warranted since hemorrhage may be intermittent. Death caused by UPE does require a large amount of clotted blood to be found in the stomach at the time of death.
Differential diagnoses include other causes of hemorrhagic diarrhea such as porcine proliferative enteritis, swine dysentery, salmonellosis, or whipworms.
Pigs suspected of having ulcers should be separated from the herd. If pale or anemic, treatment may include Vitamin K and hematinics, although treatment is of questionable efficacy. Access to fiber (hay, pasture) will sometimes aid in recovery.
Prevention is based on correcting those risk factors suspected of contributing to ulcer formation (see under Etiology). Minimizing stress and preventing out of feed events via consistent feed availability/delivery is always warranted. Altering the ration to minimize the effects of some of the possible risk factors is helpful. Changing to a more coarsely ground feed (>700 µm), including changing from a pelleted diet to a meal diet, is often recommended. The quality of the feed ingredients should be improved if some of the feedstuffs were stored for long periods or of poor quality. Successful control of swine respiratory diseases, especially swine influenza, has decreased the losses attributable to UPE on some swine farms.
See the table Diseases Associated with Hemorrhage in Intestine