The presence of van genes and virulence genes for aggregation substance (Asa-1), enterococcal surface proteins (esp), cytolysin (cylA, cylL, cylM), gelatinase (gelE), E. faecium endocarditis antigen (EfaA( fm )), hyaluronidase (hyl), and collagen adhesion (Ace) was assessed.
Two hundred and sixty-three isolates were screened for the presence of genes coding for aggregation substance (asa1), cytolysin (cylA), collagen-binding protein (ace), Enterococcusfaecalis endocarditis antigen (efaA(fs)), enterococcal surface protein (esp(fm)), gelatinase (gelE) and hyaluronidase (hyl(fm)) by polymerase chain reaction.
The lack of enrichment for asa1 or cylA among clonally unrelated E. faecalis bloodstream isolates fails to support a role for plasmid-encoded aggregation substance or cytolysin in the transition from bacteremia to endocarditis.
Extracellular toxins such as cytolysin can induce tissue damage as shown in an endophthalmitis model, increase mortality in combination with aggregation substance in an endocarditis model, and cause systemic toxicity in a murine peritonitis model.