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[[Gastric Ulceration - all species]]
[[Gastric Ulceration - all species]]
== Introduction ==
Gastic ulceration is quite common in the pig and may be seen in 50-60% of pigs arriving at slaughterhouses. It is prevalent in the UK and has been idnetified in most countries worldwide. They may cause clinical signs or death if haemorrhage or perforation occurs, however in the majority of cases they appear as an incidental finding in slaughterhouses. Ulcers are known to have economic consequences due to reduced growth rates and feed conversion rates.
== Aetiology ==
Exact cause is unknown but there are thought to be many different causes of the disease. These include, infection e.g. Candida albicans, Streptococci, Staphylococci and mixes of these, copper toxicity is also considered a possible cause; pigs are fed copper as growth promoter; 50 ppm is know to be toxic, and animals are often fed 250 ppm. Vitamin E / Selenium deficiency, feeding on concrete floors so that sand is ingested along with feed and stress are other risk factors associated with the disease. Food that is processed too finely, can exacerbate the condition but it is not known if it would cause the condition
== Clinical Signs ==
Occasionally a well-grown pig will drop dead. It will be in good body condition and often will have no concurrent illness. In less acute cases, animals may appear recumbent, breathe rapidly and may grind their teeth in pain. They will often appear generally depressed and refuse to eat or drink. Pigs may vomit and stand uncomfortably. Pain can usually be elicited upon pressure on the xiphisternum. There may be signs of melena and chronically affected animals with have a reduced growth rate.
[[Category:Gastric_Ulceration]][[Category:Gastric Diseases - Pig]]
[[Category:To_Do_-_Kate]]
== Diagnosis ==
This condition is very difficult to diagnose in the live animal and clinical signs can be vague and variable.
Anaesthesia of the pig in order to perform endoscopy is a useful diagnostic tool but only in small holdings or pet pigs as this would be uneconomical in a large farm unit.
Post mortem examination can be used for diagnosis. Signs include; lesions in the pars oesophagea (squamous or non-glandular portion), beginning with hyperkeratosis in the stratum corneum. The area will appear rough and thickened. In approximately 30% of animals, the lesion starts to erode and quite deep ulcers may develop. In a significant small number ,very deep ulcers develop and may affect virtually all of pars oesophagea.
Histologically, ulcers are large and flask-shaped ulcer with fibrin, necrosis, erosion and fibrosis at base.
== Treatment and Control ==
Supportive therapy such as fluids and blood tranfusions will help treat clinical signs. Ranitidine can be administered orally and antibiotics may be provided as a precautionary measure to prevent any secondary bacterial infections occuring. Measures to reduce stress or other risk factors should be taken.
The main control mechanism is to increase the particle size of the feed, as well as reducing stress in the herd by good husbandry measures.
== References ==
Cowart, R.P. and Casteel, S.W. (2001) An Outline of Swine diseases: a handbook Wiley-Blackwell <br>Straw, B.E. and Taylor, D.J. (2006) Disease of Swine Wiley-Blackwell<br>Taylor, D.J. (2006) Pig Diseases (Eighth edition) St Edmunsdbury Press ltd <br>
[[Category:Gastric_Ulceration]] [[Category:Gastric_Diseases_-_Pig]] [[Category:To_Do_-_Review]]