Colonization, adherence and invasion of host tissues

Bacterial adherence to host tissues is a crucial first step in the infection process. Adhesins that promote binding to eukaryotic receptors on mucosal surfaces would be expected to play a critical role in maintenance of colonization. Without specific means of attachment, enterococci would likely be eliminated by bulk flow of luminal contents through normal intestinal motility. Adherence through surface-exposed adhesins to epithelial cells, endothelial cells, leukocytes, or extracellular matrix is generally a first step in infection.  A close association is likely to exist between enterococci and its host, or the organism would be eliminated due to normal intestinal motility. Many infection-derived enterococcal isolates were found to be clonal, indicating nosocomial transmission. Moreover, a number of studies have documented patient colonization following hospital admission, and have shown that colonization with multiple resistant strains is a predisposing factor for subsequent infection. To colonize the lower bowel, enterococci must survive transit through the low pH of the stomach. Several studies have examined the acid tolerance of E. faecalis demonstrated that exposure of E. faecalis to a sub-lethal pH (pH 4.8) for 15-30 minutes protected the organism from a normally lethal challenge at pH 3.2. From these studies, it is apparent that enterococci possess the ability to withstand the low gastric pH, which would facilitate colonization. This attribute may be critical in the ability of multi-drug resistant enterococcal strains to colonize the intestinal tract and cause hospital ward outbreaks. Whether infection-derived enterococcal isolates show enhanced acid tolerance is yet to be determined. Therapy with antibiotics possessing little anti-enterococcal activity is a key predisposing factor leading to enterococcal colonization and infection. 

Studies in mice with antibiotic- induced intestinal E. faecalis overgrowth demonstrated that organisms can adhere to epithelial surfaces of the ileum, cecum, and colon. These same studies showed that enterococci possess the ability to translocate from the intestinal lumen to the mesenteric lymph nodes, liver, and spleen. 

As prior antibiotic therapy appears to be a predisposing factor for enterococcal infection, antibiotic-induced intestinal overgrowth by E. faecalis, followed by translocation of the organism into the circulation may offer one explanation for bacteremias of unknown etiology. The mechanisms responsible for enterococcal translocation are not clearly defined. One hypothesis is that enterococci are phagocytosed by tissue macrophages or intestinal epithelial cells, and are transported across the intestinal wall to the underlying lymphatic system. Failure to kill the phagocytosed organisms could then lead to systemic spread.