Virulence factors of enerococci

In order to produce infection, enterococci must be able to colonize host tissues, resist the host's non-specific and immune defense mechanisms and produce pathological changes. Enterococcal virulence factors can contribute to enterococcal disease in different ways; by enhancing colonization, adherence and invasion of host tissues, by modulation of the host immunity, and by inducing pathological changes in the host associated with increased severity of infection .

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 E. 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.

In addition to the hardiness of the genus, other components have been implicated as important factors in the sequence of events that lead to clinical human disease. Acid tolerance, mediated by any stimulus that causes an increase in proton pump activity, is thought to allow enterococci to survive passage through the stomach prior to colonization of the lower bowel.

Aggregation substance is thought to play a role in the translocation of enterococci from the intestinal lumen to the mesenteric lymph nodes, liver, and spleen. 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. Although questions concerning the pathogenicity of enterococci remain unanswered, it is clear that we are now beginning to understand the mechanisms by which this important group of microorganisms produces disease, although additional mechanisms are thought to also contribute. Another factor thought to be involved in adhesion is enterococcal surface protein (Esp), which has also been demonstrated to aid in the formation of a bacterial biofilm, and contributes to a mouse model of urinary tract infection.