Bacterial adherence to mucosal surfaces: an attribute of virulence.

Colonization of mucosal habitats is, with very few exceptions, a necessary prerequisite that must be satisfied for a bacterial organism to be virulent. The mechanism(s) whereby bacteria colonize such habitats is, for the most part, by association with the mucosa and proliferation at that site. However, the precise mechanism(s) of association is not known for most organisms. Direct adherence to the mucosal surface of the small intestine by some enterotoxigenic strains of Escherichia coli (ETEC) has been demonstrated both in vivo and in vitro. Specific surface appendages (pili) on the bacterial cell surface facilitate the direct attachment of bacteria to microvilli and as such have been termed adhesins. The adhesins of ETEC that cause diarrheal disease in pigs have been most extensively studied. Two adhesins, K88 and K99, are genetically encoded on plasmids while a third one, 987P, appears to be encoded on the chromosome. All three adhesins are composed of identical repeating protein subunits with molecular weights of 18,100-26,000 that undergo specific aggregation to form large polymers. These polymers are the active adhesins and appear as pili (synonym: fimbriae) when observed in the electron microscope. The function of these adhesins has been established by construction of mutants or plasmidless strains that do not produce the adhesin and by reintroduction of the adhesin genes back into the mutants. Only cells that produce the adhesins colonize and adhere to the mucosa of the pig intestine in vivo and thus produce diarrheal disease. The interaction of adhesin with the mucosal surface is mediated by specific receptors. Current data indicate that these receptors are glycoconjugates.