Gastric ulceration of the pars oesophagea (a part of the stomach which is an extension of the esophagus or gullet) is important in the pig, but ulceration of the glandular part of the stomach also occurs. It occurs worldwide and affects weaners, growers / finishers (screams, sows) and effects paleness, weight loss, sudden death, teeth grinthing, Vomit, black dung.
- Causes of Gastric ulcers >
- Effects of Gastric ulcers >
- Diagnosis of Gastric ulcers >
- Treatment & Control of Gastric ulcers >
Causes of Gastric ulcers
The cause of both types of gastric ulceration is unknown. The pig helicobacter, H. heilmannii has present in the stomach and may be involved. Other bacteria ferment carbohydrate, produce organic acids and predispose the 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 over crowding, increase the incidence of gastric ulceration in pigs. Hyperkeratosis (rough ning and discoloration) 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.
Effects of Gastric ulcers
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 intra gastric 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 melena (digested blood in the faeces), passing dark, dry feces, with a loss of appetite and reduce growth rate.
The sub-clinical form is most commonly seen at slaughter. Significantly Affected pigs grow more slowly than unaffected animals especially when scarring of the esophagus has occurred.
Diagnosis of Gastric ulcers
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. Anesthesia followed by endoscopy can allow the cardia (upper part of the stomach) to be inspected. Clearly ulceration can be seen, but hyperkeratosis (an early change) may not be detectable and is visible only at post-mortem examination.
Pigs which have died as a result of haemorrhage from an ulcer are pale, the stomach is often distanced ended 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 or gastric ulceration. The pars oesophagea is normally pearly white but becomes thickened, hardened, rough and yellow-brown, then light brown with superficial erosion and sloughing until it finally ulcerates.
Treatment & Control of Gastric ulcers
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 crowding on, using proper ventilation and also by reducing the growth rate of young stock growth promoters or omit from the rations and by increasing fiber 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 5mg/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 um for a three week period, after the events likely to cause early lesions, and ensuring that the ration if fed as meal rather than as a pellet. Even if developed ulcers may resolve this feeding regime is adopted. Particle size pellets may also be increased. The pH of whey should be checked and very acid whey should not be fed.
