Oedema disease: a review of the disease and control and preventative measures

02 May 2020
10 mins read
Volume 25 · Issue 3
Figure 4. Nervous signs (lateral position, paddling limbs) in a pig with oedema disease.
Figure 4. Nervous signs (lateral position, paddling limbs) in a pig with oedema disease.

Abstract

Oedema disease is caused by a toxin produced by Shiga toxin-encoding Escherichia coli. The susceptibility of pigs to oedema disease is often increased shortly after weaning due to stress and an increase of presence of specific receptors, susceptible for F18, needed for the colonisation of the small intestine and also due to change of feed, mainly from sow milk-based carbohydrates (milk sugar) to starch from grains, which are not so easily digested. The correct diagnosis of oedema disease is important in order to determine the control or preventative measures that can be implemented on farm. Vaccination has been shown to be the most successful method for preventing clinical oedema disease and a reduction in mortality. Vaccination can also have a positive effect on the reduction of antibiotic usage and ZnO on a farm, which is extremely important in ensuring livestock industries are meeting reduction targets. By ensuring effective hygiene and biosecurity measures are in place alongside vaccination, the negative impacts of oedema disease on production can be minimised.

Escherichia coli is a Gram-negative bacteria belonging to the family Enterobacteriaceae and is the causative agent of a wide range of diseases in pigs, including neonatal diarrhoea, post-weaning diarrhoea (PWD) and oedema disease (OD), which are important causes of death occurring worldwide in suckling and weaned pigs respectively (Zimmerman et al, 2019). OD is also known as ‘bowel oedema’ or ‘gut oedema’ because oedema of the submucosa of the stomach and the mesocolon is often a prominent feature of the disease. Shiga toxin encoding E.coli (STEC) strains result in release of Shiga toxin type 2e (Stx2e) which is the causative agent of OD in weaned piglets, with clinical signs usually becoming apparent around 2 weeks post weaning (Zimmerman et al, 2019). However, clinical problems and mortality can be observed during all nursery periods. Prevalence of STEC has been reported in various studies worldwide and has been shown to vary greatly, usually depending on genetics, farm management and antibiotic use in the post-weaning period (Tseng et al, 2014). Strategies to control OD include implementing a vaccination protocol against OD, which has been shown to be effective in reducing clinical cases and mortality caused by the disease.

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