Oedema disease is associated with metabolic acidosis and small intestinal acidosis.

Limited information is available about the pathogenesis and pathophysiology of oedema disease (OD). Oedema disease is caused by specific enterotoxemic Escherichia coli (SLTIIv-toxin producing) strains; however, the same strains are also found in non-afflicted pigs. Furthermore, it is unclear how the 80 kDa SLTIIv-toxin can pass the intestinal barrier. In the present paper, piglets showing signs of acute OD were anaesthetised, instrumented and cardiovascular and intestinal parameters were determined at 0, 1, 2 and 3 hours. Healthy piglets from the same herd were used as a control. Cardiac output, blood pH and bicarbonate, small intestinal intramucosal pH, and (pulmonary) blood pressure were significantly lower in OD-pigs than in control pigs. It is concluded that OD is associated with metabolic and intestinal acidosis. Intestinal acidosis is known to increase macromolecular permeability. This suggests that once OD has developed, influx of SLTIIv-toxin into the blood stream is facilitated, thus perpetuating the disease. Since intestinal permeability appears to be central in OD, it is argued that post-weaning events increase intestinal permeability and predispose individuals to OD.