Studies of the interplay between genetic and passive factors important for the protection of the neonatal pig from infection by enterotoxigenic K88-positive Escherichia coli

• Main Author: Sellwood, R.
• Published: University of Reading 1983
• Subjects: 636.089; Pig bacterial infection
• Online Access: http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.351126

An outbreak of neonatal diarrhoea was investigated in a herd of known susceptibility to infection by K88- positive Escherichia coli. The probable cause of the majority of diarrhoea cases was identified as a K88- positive E. coli strain. Diarrhoea was confined to susceptible piglets born to resistant sows. Susceptible sows protected their susceptible offspring and resistant piglets were unaffected. Potential protective mechanisms of the colostrum of susceptible sows were compared to the same properties in colostrum of resistant sows. Colostrum from susceptible sows (a) inhibited the binding of K88 antigen to intestinal epithelial cell brush borders, and (b) opsonized E. coli strain G205 and promoted in-vitro killing by porcine neutrophils significantly better than colostrum from resistant sows. Fractionation of colostrum by gel filtration and ion-exchange chromatography permitted identification of the immunoglobulin classes most efficient in both these activities. Both IgM and IgA, but not IgG, inhibited binding of K88 antigen to brush borders and opsonic activity was predominantly mediated by IgM. The importance of opsonic activity depends on the ab.ility of neutrophils to phagocytose bacteria within the intestinal lumen. In intestinal ligated loop experiments emigration of neutrophils into the lumen and phagocytosed bacteria were demonstrated by light microscopy and scanning and transmission electron microscopy. Neutrophil emigration only occurred when piglets had received maternal antibody_ No equivalent neutrophil emigration was observed in susceptible .piglets deprived of colostrum. There was also little or no neutrophil response in colostrum-fed resistant piglets probably du~ to a lower concentration of bacterial antigens close to the epithelial cell surface .or lack of specific antibody. Experiments to determine the numbers of organisms killed by neutrophils in the intestinal lumen failed to demonstrate any reduction, attributable to phagocytosis, in viable K88-positive E. coli.