Age affected: Weaners, growers/finishers (gilts, sows).
Causes: Dietary factors; stress.
Effects: Paleness, weight loss, sudden death, teeth grinding, vomiting, black dung.
Gastric ulceration of the pars oesophagea (a part of the stomach which is an extension of the oesophagus or gullet) is important in the pig, but ulceration of the glandular part of the stomach also occurs. The cause of both types of gastric ulceration is not clear. The pig helicobacter, H. suis, is present in the stomach is capable of causing gastritis and ulceration, possibly by means of γ glutamyl transpeptidase. Other bacteria ferment carbohydrate, produce organic acids and predispose to pars oesophagea to ulceration. Gastric ulceration has been observed in swine fever and TGE, but in the glandular area, not the pars oesophagea. Pneumonia and infection by the stomach worm, Hyostrongylus rubidis, may predispose to gastric ulceration. Nutrition may play some part in the condition and finely-ground pelleted feeds may also be involved. They may not initiate the condition, but play a major part in the maintenance and exacerbation of the lesions. Stresses such as transport, starvation, mixing and overcrowding, increase the incidence of gastric ulceration in pigs. Hyperkeratosis (roughening and discolouration) or the pars oesophagea leads to erosion and then to ulceration. Ulcers may remain open and blood vessels may rupture to cause death by bleeding. Healing may occur at any stage but is accompanied by scarring if ulceration has occurred.
The most important infectious component of porcine gastric ulceration is H. suis, and it is present in saliva and in faeces of infected pigs. Infection is oral, following contact with carrier pigs. Many of the other possible factors involved in gastric ulceration are not transmissible, but may influence the occurrence of the condition in successive batches.
Animals with gastric ulceration are often found dead in good condition. Animals of any age may be affected, but the condition is particularly common in sows before and after parturition and rapidly growing pigs between 20 and 400 kg. Animals which survive and acute intragastric haemorrhage are unable to rise, breathe rapidly and may grind their teeth in pain. They refuse to eat or drink, the body temperature is low and all visible mucous membranes (gums, vulva) are cold and pale. Affected pigs may vomit and stand with a rigid back. Pain can be elicited by pressure at the xiphisternum. Sub-acute cases may show intermittent melaena (digested blood in the faeces), passing dark, dry faeces, with loss of appetite and a reduce growth rate. The sub-clinical form is most commonly seen at slaughter. Affected pigs grow significantly more slowly than unaffected animals especially when scarring of the oesophagus has occurred.Gastric ulceration is difficult to diagnose in the live pig. Pale pigs with tarry blood in the faeces for 38 days with no fever or other signs may have gastric ulceration. In younger pigs, proliferative haemorrhagic enteropathy produces similar signs. Raised plasma pepsinogens (stomach enzymes) may suggest the condition. Gastric ulceration must be differentiated from swine dysentery and salmonellosis. Anaesthesia followed by endoscopy can allow the cardia (upper part of the stomach) to be inspected. Ulceration can be clearly seen, but hyperkeratosis (an early change) may not be detectable and is only visible at post-mortem examination.
Pigs which have died as a result of haemorrhage from an ulcer are pale, the stomach is often distended with clotted blood and the intestines are filled with blood which may be altered. The haemorrhage may be traced to the edge or floor of an acute ulcer or to the side of a chronic one. Perforation may also occur. Ulcers may heal with scarring. Pigs which have died or been slaughtered may often have early lesions of gastric ulceration. The pars oesophagea is normally pearly white but becomes thickened, hardened, rough and yellow-brown, then light brown with superficial erosions and sloughing until it finally ulcerates.
Treatment by blood transfusion or intravenous fluid therapy can relieve the clinical signs and ranitidine syrup may be given orally at 300 mg/sow/day. Antimicrobial cover may also assist the recovery of valuable individual animals. Gastric ulceration may be reduced by removing stress, relieving overcrowding, using proper ventilation and also by reducing the growth rate of young stock of omitting growth promoters from the rations and by increasing fibre levels in the diet, particularly by the use of oats or sugar beet pump. Zinc, selenium and vitamin E levels should be supplemented if inadequate. Specific measures shown to reduce ulceration include the use of melatonin 5 mg/kg in feed, methionine supplementation and the inclusion of straw. The most important preventive measure is to increase the particle size of the ration to 750 µm for a three week period, after events likely to cause the early lesions, and ensuring that the ration if fed as meal rather than as a pellet. Even developed ulcers may resolve if this feeding regime is adopted. Particle size in pellets may also be increased. The pH of whey should be checked and very acid whey should not be fed.
Helicobacter suis can colonise humans and may be present on meat. Normal hygienic precautions may reduce the possibility of infection.