Nursing litters of vaccinated (K88 antigen) and non-vaccinated gilts as well as weaned piglets, which had recovered from natural colibacillosis, were exposed to Escherichia coli O149: K91(B), K88ac(L) orogastrically and 3-4 h after exposure a proportion of each group was killed for adhesion studies; others were kept for clinical observations. From killed piglets duodenal contents were collected and after washing of the duodenum by standardised techniques it was homogenised. Viable counts of E coli O149 in these specimens were carried out and compared. Colicounts in the duodenal contents and in the homogenate of washed duodenum of naturally infected piglets were also compared. There was less than tenfold difference in counts of K88-positive E coli between duodenal contents and washed duodenum of piglets which were (A) naturally infected, (B) colostrum deprived and experimentally infected, or (C) were from colostrum fed groups where those litter mates which were kept for clinical observation died of colibacillosis. There was 10(3)-10(5)-fold difference in E coli O149 counts between comparable specimens from piglets which (a) recently recovered from K88-positive E coli infection at the time of oral challenge or (b) were from colostrum fed groups where those litter mates which were kept for clinical observation survived oral challenge. It is concluded that adhesion of K88-positive E coli to the epithelium of the anterior small intestine of the pig is a feature of natural as well as experimental colibacillosis. Such adhesion may be prevented by (i) earlier natural infection of K88-positive E coli or (ii) by the ingestion of colostrum of K88 antigen vaccinated dams.
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