**8. Virulence factors**

Most number of virulence factors are present in human pathogenic enterococci followed by animal pathogenic enterococci.

Variable factors: Production of bacteriocins or enterocins, is one process that depends on the environment. When there is a harsh environment and there is competition for survival, enterococci are seen to produce enterocins that are capable of killing *Staphylococcus aureus*, Listeria and clostridium species.

Antibiotic resistance is another factor that is dependent on the environment. In a hospital environment with antibiotic pressure, enterococci rapidly acquire and activate genetic elements like plasmids with transposons. They are capable of conjugation based on a pheromone induced system that does not depend on pili. Pheromones released by plasmid free cells are taken up by those with plasmids, leading to upregulation of synthesis of specific aggregatory proteins that help these bacteria to attach to each other for transfer of genetic material. The plasmid transferred contains not only conjugatory genes, but also genes responsible for antibiotic resistance and virulence factor production. One such plasmid induced by pheromones and extensively studied is pAD1. It carries the Tn917 transposon and the Tn916 transposons that are integrated into the recipient cell after conjugation. Tn916 is known to code for Tetracycline resistance in addition to be actively involved in conjugation [15].

Constant virulence factors:

	- a.Ace: Adhesion of collagen of enterococci, seen in *E. faecalis* isolated from infective endocarditis.
	- a.Cytolysin or hemolysin which is bactericidal for other bacteria and is haemolytic.
	- b.Hyaluronidase breaks down the mucopolysaccharide in connective tissue helping spread of enterococci, a feature shared with other streptococci.
	- c.Gelatinase and serine protease break down proteins and have a role in biofilm formation also. They are produced when the quorum sensing system is activated and involves the faecal streptococci regulator (*fsr*) gene. Mutations in this gene reduce biofilm formation. All infective endocarditis isolates were seen to have this gene while from stool samples, only 53% had this gene [15].
