Difference between revisions of "Gastric Ulceration - Pig"

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[[Gastric Ulceration - all species]]
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== Introduction ==
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* Gastic ulceration is quite common in the pig- May be seen in 50-60% of pigs arriving at slaughterhouses.
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* Has serious economic consequences.
  
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Gastric 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 identified in most countries worldwide. The ulcers 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.
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*'''Clinical'''
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** Occasionally a well-grown pig will drop dead.
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*** Deep ulcers have eroded into a blood vessel, causing massive haemorrhage into the [[Forestomach - Anatomy & Physiology|stomach]] from and producing death very rapidly.
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** If long standing ulcers do not result in death, they do produce pain and discomfort.
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*** Give low growth rate and poor feed conversion.
  
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== Aetiology ==
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*'''Pathogenesis'''
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** Gastric ulceration is associated with modern pig rearing, but the exact cause is unknown.
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** Causes are associated with gastric hyperacidity, and gastric ulceration is probably a multifactorial disease.
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** The following are suggested as possible causes:
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*** Infection, e.g. ''Candida albicans'', ''Streptococci'', ''Staphylococci'' and mixes of these.
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*** Copper toxicity- this is probably more significant.
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**** Pigs are fed copper as growth promoter; 50 ppm is know to be toxic, and animals are often fed 250 ppm.
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*** Vitamin E / Selenium deficiency.
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*** Feeding on concrete floors.
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**** Sand is licked up whe pigs eat.
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*** Feeding finely milled cereal.
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*** Stress
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*** Possibly genetic factors.
  
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Exact cause is unknown but there are thought to be many different causes of the disease. These include, infection e.g. ''[[Candida spp.]]'', [[:Category:Streptococcus species|Streptococci]], [[:Category:Staphylococcus species|Staphylococci]] and mixes of these, [[Copper Toxicity|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 it.
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*'''Pathology'''
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** Most commonly affects pars oesophagea (squamous or non-glandular portion).
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** Starts with hyperkeratosis in the stratum corneum
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*** Appears rough and thickened
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*** May stop at this stage.
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** In approximately 30% of animals, the lesion starts to erode and quite deep ulcers may develop.
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** In a significant small number ,very deep ulcers develop and may affect virtually all of pars oesophagea.
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** Histologically, ulcers are large and flask-shaped ulcer with fibrin, necrosis, erosion and fibrosis at base.
  
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== Clinical Signs ==
 
  
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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 will have a reduced growth rate.
 
  
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== Diagnosis ==
 
  
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This condition is very difficult to diagnose in the live animal and clinical signs can be vague and variable.
 
  
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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.
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[[Category:Gastric_Ulceration]][[Category:Pig]]
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[[Category:To_Do_-_Clinical]]
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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.
 
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Histologically, ulcers are large and flask-shaped with fibrin, necrosis, erosion and fibrosis at base.
 
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== Treatment and Control ==
 
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Supportive therapy such as fluids and blood transfusions 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 occurring. Measures to reduce stress or other risk factors should be taken.
 
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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.
 
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<big>Also see '''[[Gastric Ulceration - all species]]'''</big>
 
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== References ==
 
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Cowart, R.P. and Casteel, S.W. (2001) An Outline of Swine diseases: a handbook Wiley-Blackwell
 
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Straw, B.E. and Taylor, D.J. (2006) Disease of Swine Wiley-Blackwell
 
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Taylor, D.J. (2006) Pig Diseases (Eighth edition) St Edmunsdbury Press ltd
 
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{{review}}
 
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{{OpenPages}}
 
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[[Category:Gastric_Ulceration]] [[Category:Gastric_Diseases_-_Pig]] [[Category:Expert_Review - Farm Animal]]
 

Revision as of 22:54, 28 June 2010

Gastric Ulceration - all species

  • Gastic ulceration is quite common in the pig- May be seen in 50-60% of pigs arriving at slaughterhouses.
  • Has serious economic consequences.
  • Clinical
    • Occasionally a well-grown pig will drop dead.
      • Deep ulcers have eroded into a blood vessel, causing massive haemorrhage into the stomach from and producing death very rapidly.
    • If long standing ulcers do not result in death, they do produce pain and discomfort.
      • Give low growth rate and poor feed conversion.
  • Pathogenesis
    • Gastric ulceration is associated with modern pig rearing, but the exact cause is unknown.
    • Causes are associated with gastric hyperacidity, and gastric ulceration is probably a multifactorial disease.
    • The following are suggested as possible causes:
      • Infection, e.g. Candida albicans, Streptococci, Staphylococci and mixes of these.
      • Copper toxicity- this is probably more significant.
        • 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.
        • Sand is licked up whe pigs eat.
      • Feeding finely milled cereal.
      • Stress
      • Possibly genetic factors.
  • Pathology
    • Most commonly affects pars oesophagea (squamous or non-glandular portion).
    • Starts with hyperkeratosis in the stratum corneum
      • Appears rough and thickened
      • May stop at this stage.
    • 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.
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