Bowel oedema (oedema disease)

calendar icon 8 November 2018
clock icon 7 minute read

Background and history

This is also called bowel disease or gut oedema. It is caused by certain serotypes of E. coli bacteria that produce a powerful toxin (verotoxin). These toxins damage the walls of small blood vessels including those in the brain and cause fluid or oedema to accumulate in the tissues of the stomach and the large bowel. Damage to the blood vessels in the brain results in some of the characteristic signs. The specific E. coli are described as O138, O139 and O141. Disease is generally seen 1 to 4 weeks after weaning, the peak being at 10 days. It was very common when pigs were weaned at 5 to 8 weeks of age. Since weaning ages have reduced to 17 to 26 days and starter diets have been improved the disease in its classical form is rarely seen. The E. coli bacteria attach themselves to the finger-like villi in the anterior small intestine and produce the toxins. This mechanism is similar to that which occurs in post-weaning diarrhoea associated with different strains of E. coli. During sucking the secretory IgA immunoglobulin component in milk prevents the bacteria adhering. After weaning when the IgA has disappeared the pigs becomes susceptible to disease.

Clinical signs

Acute disease

Sometimes the only sign is a good pig found dead 1 to 4 weeks post weaning. Recovery in the few pigs that do not die takes up to 2 to 3 weeks. Certain breeds of pigs may be associated with disease suggesting a genetic predisposition. The temperature is usually normal.

Typically, live affected pigs show:

  • A staggering gate.
  • Incoordination.
  • Puffy eyelids giving a sleepy appearance.
  • An abnormal high pitched squeak.
  • Pigs stop eating.
  • In the later stages become partially paralysed and go off their legs.
  • Sometimes with nervous symptoms. Muscle twitching, fits.
  • Diarrhoea is not a feature.
  • Breathing difficulties become evident.
  • The damage to the brain is irreversible and most pigs die.
  • Lameness.


This is made from the typical clinical signs, the sudden appearance of disease after weaning, post-mortem examinations showing oedema of the greater curvature of the stomach wall, coiled colon, and eyelids and isolation of the haemolytic E. coli serotypes from the duodenum (anterior small intestine).


Associated with weaning and changes of diet.


  • This can be difficult and unrewarding.
  • Certain types of breeding animals may be more susceptible and mortalities in such cases may rise to 25% or more.
  • Reduce piglet exposure to the E. coli during sucking. Adopt all the procedures in the farrowing house for the control of scour in the sucking pig.
  • Consider the use of an autogenous vaccine in sows to raise colostral antibodies and block out infection in the sucking pig. This has been effective on a few farms.
  • Assess the effects of no creep feeding pre-weaning.
  • Restrict feed intake post-weaning.
  • Assess the effects of different diets and feeding routines.
  • Reduce the nutrient composition of the diet by increasing the fibre content by 10 to 15%.
  • If the problem is a major one and it continues, consider a change of genotype. Some strains of pig are more resistant than others.
  • Lower or alter the age of weaning.
  • Alter the environment at weaning time.
  • Asses the effects of adding 3% of milk powder to the diet.
  • Assess the effects of zinc oxide to the diet at a level of 2500ppm zinc.


By the time the clinical signs are seen it is often too late and most pigs die. Treatment routines are aimed at preventing the organism establishing itself and also reducing the weight of infection. The general principles of controlling coliform infections and post-weaning diarrhoea should be followed.

  • Isolate the organism and determine the antibiotic sensitivity.
  • Identify the stage (e.g. 10 days post-weaning) when disease first appears and apply either in-feed or water medication 3 to 5 days before this.
  • In-feed antibiotics of value include apramycin 100g/tonne, framycetin 100g/tonne, neomycin 163g/tonne. Alternatively apramycin, neomycin or trimethoprim/sulpha can be used in the water.
  • Individual treatments give a poor response but flunixin will help to reduce the effects of toxins and diuretics can be used to remove fluid.

It must be admitted however that the disease is most difficult to deal with and often preventative medication and treatment are unsuccessful.

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