Infection with Clostridium perfringens type C leads to necrotic enteritis in newborn piglets within the first hours to days of life. The susceptibility to the disease (morbidity) is 15%–80% and the losses (mortality) can be up to 100%. The cause factors for the high susceptibility of neonatal piglets to clostridia are the trypsin inhibitors present in colostrum and a high gastric pH. Trypsin is an enzyme involved in the digestion of protein that has also been shown to break down Clostridium perfringens ß-toxins. The presence of trypsin inhibitors allows the ß-toxins to freely enter the digestive tract where they can cause harmful effects. The trypsin inhibitors in colostrum protect the colostral antibodies, but they also inhibit the natural protection of piglets against Clostridium perfringens type C.

As a result of the trypsin inhibitors, necrotic enteritis occurs almost exclusively in the suckling period, Clostridium perfringens type C produces ß-toxins that are primarily responsible for necrotic enteritis. The toxins cause necrosis of the villi and the deeper layers of the mucosa. This may lead to a leakage of blood into the intestines. Depending on the amount of toxin formed, the disease will progress in different ways. In general there is impaired nutrient absorption, diarrhoea and an imbalance of the normal gut flora (microbiota). In addition, affected piglets have reduced appetite, rough haircoat and are lethargic. In cases when the disease is not lethal, the piglets show signs of wasting. There are three different forms of NE: peracute, acute and chronic: