Stomach (gastric) ulcers
Age affected: Growers/ finishers, gilts, sows.
Causes: Dietary factors e.g., fine particles, low fibre, high energy; irregular feeding; stress; Helicobacter bacteria.
Effects: Pale skin, black tarry dung, vomiting blood, weight loss, sudden death.
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 unknown. The pig helicobacter, H. suis, is present in the stomach and may be involved, together with Fusobacterium gastrosuis, another organism found in the early lesions.
Other bacteria ferment carbohydrate, product organic acids and predispose the parts 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. The earliest lesions are hyperkeratosis (roughening and discolouration) of the pars oesophagea followed by erosion and then by 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.
Mode of transmission
As the causes of the condition are not yet completely clear, gastric ulceration of the pars oesophagea appears to depend on husbandry and management factors which are associated with its development. Infection with H. suis is involved and it is transmitted to pigs by the oronasal route. The organism is shed in saliva and in faeces and contact with these sources results in infection. Infection is widespread, so exposure normally occurs relatively young and increases with age.
Although it can infect other species, including humans, the part they play in its spread is not yet fully understood. The spread of the other bacteria which may be involved has not yet been investigated. Other infectious diseases which cause ulceration of the glandular part of the stomach are spread to pigs by the routes specific for those disease agents. The manahement factors are not transmissible and even feeds which provoke the condition on one farm may not do so on another.
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 in rapidly growing pigs between 20 and 40 kg.
Animals which survive the 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 (rear end of the breast bone). Sub-acute cases may show intermittent melaena (digested blood in the faeces), passing dark, dry faeces, with loss of appetite and a reduced 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 3-8 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 by 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 and black. The haemorrhage may be traced to the edge or floor of an acute ulcer or to the sides of a chronic one. Perforation may also occur, leaking contents into the peritoneal cavity. 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. Ulcers of the glandular parts are usually less severe, but in animals with TGE, swine fevers and salmonellosis, there may even be haemorrhage and congestion.
Treatment and prevention
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 be reducing the growth rate of young stock by omitting growth promoters from the rations and by increasing fibre levels in the diet, particularly by the use of oats or sugar beet pulp. 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 is 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.
H. suis is one of the commonest helicobacters in humans where H. pylori is a well-known cause of gastric ulceration. It may be involved in human disease.