Different pig phenotypes affect adherence of Escherichia coli to jejunal brush borders by K88ab, K88ac, or K88ad antigen

Abstract

At least five different porcine phenotypes were distinguished with the three serological variants of the K88 antigen in the brush border adhesion test. Pigs of one phenotype (A) are susceptible to adherence of all three variants, pigs of three phenotypes are susceptible to only two (B and C) or one (D) of the K88 variants, and pigs of one phenotype (E) are entirely resistant to adhesion of K88 antigen. Preincubation of type A brush borders with an excess of purified K88ad antigen did not interfere with the adhesion of K88abor K88ac-positive Escherichia coli, whereas in most cases K88ab and K88ac antigen completely blocked the adhesion of K88ad-positive E. coli. Likewise, K88ab antigen blocked the adhesion of K88ac-producing E. coli to both type A and type B brush borders, and vice versa.

Effect of experimentally-induced villus atrophy on adhesion of K88ac-positive Escherichia coli in just-weaned piglets

“…No adhesion, however, was observed in specimens with severe atrophic villi (smaller than 120 Bm). Since K88-positive ETEC specifically adhere to brush border membranes from genetically-susceptible pigs, this absence of in vivo adhesion on these severe shortened villi could have indicated that piglets had a non-adhesive phenotype (Bijlsma et al, 1982;Sellwood, 1983 ). The vitro adhesion assay, however, revealed attachment of K88ac ETEC to the atrophic villi.…”

“…After gently mixing villi and bacterial suspension for 1 h at room temperature, some villi were removed with a pipette, placed under a cover slip and examined by light microscopy at magnification × 600. When no adhesion was observed piglets were considered as genetically resistant (Bijlsma et al, 1982;Sellwood, 1983). When adhesion occurred, however, it was quantified by counting the number of visible bacteria adhering along 50 pm villus brush border at 5 different places villus-1 (250 pm villus-') and on 5-6 villi small intestinal segment-'.…”

Salivary interactions with homologous and heterologous strains of oral streptococci and epithelial cells

“…Bacterial strainr -Strains of oral streptococci were isolated by sampling with a sterile cotton swab from the tongue and buccal mucosa of four subjects (2 men, subjects A and B, and 2 women, subjects C and D, aged [25][26][27][28][29][30][31][32][33][34][35], and cultivated on Mitis-Salivarius agar (MS) (Difco, Detroit, USA). After 48 h incubation at 37"C, in an atmosphere of 95% N, and 5% COz, a total of 20 colonies resembling Streptococcus salivarius and Streptococcus mitior were transferred to new MS agar plates and further to Brain Heart Infusion medium (BHI, Difco).…”

Preface

“…The genes responsible for production of intestinal receptors belong to the TF blood group linkage group (Gibbons et al, 1977). Receptor functions seem to be dependent on the "b", "c" and "d" components, and in genetically resistant piglets the receptors are usually absent for both of these components of the K88 variants (Hohmann and Wilson, 1975;Bijlsma et al, 1982). In vitro adhesion tests have revealed a polymorphism of intestinal receptors for K88 and indicated that there are 5-6 different adhesion patterns (A-F) among piglets according to the K88ab, K88ac and K88ad variants (Bijlsma et al, 1982;Rapacz and Hasler-Rapacz, 1986;Billey et al, 1998).…”