Novel mucosal anti-microbial functions interfering with the plasmid-mediated virulence determinants of adherence and drug resistance.

Mucosal antibodies in vivo and in vitro interfere with the stability of plasmids coding for important virulence determinants in porcine enteropathogenic E. coli (EEC), such as the adhesion determinants K88ab and K88ac. The effector antibody is not directed against K88 antigens and is not serotype specific, but an antigen common to K88+ strains is implicated. Further lack of pathogen specificity is exemplified by antibody elimination of the more recently discovered K88ad plasmid. Antibodies that interfere with K88 plasmids do not affect K99, which now appears as an alternative adhesion factor in porcine enteropathogenic E. coli. This plasmid can be eliminated, however, by antibodies having K99 specificity. In extending the studies to drug-resistance plasmids, further evidence has emerged that mucosal antibodies may assist in host control of the reservoir of R factors in the intestinal microflora. A major effector mechanism is that secretory IgA and IgM antibodies from orally immunized pigs can block the transfer of R factors between donor and recipient strains of E. coli.