Abstract

Enterotoxigenic E. coli (ETEC) strains are an important cause of diarrhoea in young animals and children. These strains produce enterotoxins which stimulate small intestinal electrolyte and fluid secretion. Most ETEC strains possess long, threadlike protein polymers (fimbriae) on their surface, which mediate attachment to specific receptors or receptor sites on villous enterocytes. Specific adherence plays two important roles in the pathogenesis of diarrhoea. It allows ETEC to resist the natural flushing mechanisms in the intestine and to colonize the small gut. But it also facilitates the interaction between ETEC elaborated enterotoxins and small intestinal epithelial cells. Although a wide variety of fimbrial adhesins have been reported (1), K88 fimbriae possessing ETEC strains are most commonly isolated from cases of diarrhoea in just-weaned piglets. The K88 antigen exists in 3 serological variants: K88ab, K88ac and K88ad (2). In piglets, presence or absence of receptors or receptor sites for these variants is genetically determined (3). The genetic susceptibility of piglets to adhesion of K88 ETEC to their villi can only be identified using a jejunum resection or biopsy technique in combination with an in vitro adhesion assay (4,5). In this study we investigated whether the in vitro villous adhesion could be replaced by an easier to perform buccal cell adhesion assay.

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