Ulcers affect the pars esophagea in pigs and cause sporadic cases of acute gastric hemorrhage resulting in death or slow growth due to chronic ulceration.

Etiology

The specific causes are unknown. Ulcers are seen in pigs of all ages but are most common in growing pigs (100–200 lb [45–90 kg]) fed pelleted feed or finely ground rations, and also in pigs fed large quantities of skimmed milk or whey. It is thought that promotants of hyperacidity may contribute to ulcer development. A combination of finely ground feeds, transportation, hot weather, deprivation of feed and water, and mixing with unfamiliar pigs results in a significant increase in the incidence of gastric ulcers in rapidly growing pigs. Variability in daily feed intake secondary to a systemic illness, particularly pneumonias, also result in an increased incidence of ulcers. This condition is particularly significant in pigs gathered for slaughter at abattoirs, especially those transported long distances.

Clinical Findings

In the peracute form, the pig dies quickly; it is found dead with paleness as the only sign. In the acute form, hemorrhage results in anorexia, weakness, anemia, and black, tarry feces; death can occur in hours or days. In the chronic form, unthriftiness, anemia, and black, tarry feces are characteristic; the pig may survive for several weeks. Pigs with the subclinical form may not reach maturity at the expected time; in these pigs, the ulcer usually heals and a scar remains. In some herds, up to 90% of pigs may be affected; in other herds, the incidence is sporadic. In findings at abattoirs, the incidence of ulcers may be quite high in pigs that have grown normally, although the lesion may have developed in some during transport. Clinical disease apparently develops only after hemorrhage of the ulcer.

Lesions

The typical terminal lesion is found in the gastric mucosa near the esophageal opening in a rectangular area of white, glistening, nonglandular, squamous epithelium. It is common to find a crater ≥2.5–5 cm in diameter encompassing the entrance of the esophagus. The crater appears as a cream or gray, punched-out area and may contain blood clots or debris. In acute hemorrhage, the stomach and upper small intestine contain dark blood. Earlier lesions are characterized by hyperkeratosis and parakeratosis of the squamous epithelium in the area of the esophageal opening into the stomach. Later, the proliferative lesion erodes to form the ulcer. The healed ulcer appears as a stellate scar.

Diagnosis and Treatment

Appearance in a pen of 1 or 2 listless, anorectic pigs that show weight loss, anemia, dark feces, and sometimes dyspnea is suggestive of gastric ulceration, as is the sudden death of an apparently healthy pig. Differential diagnoses include hemorrhage of the bowel, eperythrozoonosis, Hyostrongylus rubidus infection, and porcine enteropathy.

No economically feasible treatments are currently available. Palliative care—removing the affected pig from the pen and feeding a coarse and fibrous diet—can be attempted. Early marketing of affected pigs should be considered. Controlling chronic respiratory disease is important. Feeding meal rather than pellets, with a recommended particle size ≥600–700 μm in diameter, is of value but may have a negative effect on feed conversion. Strategic use of such diets during stages of production that are at higher risk is useful.

Last full review/revision March 2012 by John Deen