In order to produce infection, enterococci must be able to colonize host tissues, resist the host's non-specific and immune defence mechanisms and produce pathological changes. With regard to colonization of host tissues, adherence assays have shown that enterococci can attach to intestinal and urinary tract epithelial cells and heart cells by means of adhesins expressed on the bacterial surface. The expression of these adhesins by enterococci has further been shown to be affected by bacterial growth conditions. In addition, the adherence of Enterococcus faecalis to renal tubular cells in vitro is enhanced if the organisms produce aggregation substance, a proteinaceous surface material that aggregates donor and recipient bacteria to facilitate plasmid transfer. Bacterial growth conditions also affect the interaction of enterococci with polymorphonuclear leucocytes (PMNLs), with serum-grown organisms showing less association with PMNLs than organisms grown in broth. Efficient killing of enterococci by PMNLs in vitro requires the presence of serum complement proteins and is enhanced by anti-enterococcal antibodies. Enterococci produce a number of factors that may be associated with pathological changes in the host. Both sex pheromones and plasmid-encoded pheromone inhibitors produced by E. faecalis are chemotactic for PMNLs in vitro, and may mediate, at least in part, the inflammatory response often associated with enterococcal infection. E. faecalis may also produce a plasmid-encoded haemolysin, which is associated with increased severity of infection. In addition, enterococci are capable of inducing platelet aggregation and tissue factor-dependent fibrin production, which may be relevant to the pathogenesis of enterococcal endocarditis.(ABSTRACT TRUNCATED AT 250 WORDS)