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.
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.