**8. Infective endocarditis**

Enterococci are the second most cause of infective endocarditis. Endocarditis caused by VRE faecalis causes GI or GU manipulation, damaged mitral or aortic valve infections, liver transplantation whereas VRE faecium endocarditis is associated with infection of tricuspid valve [36]*. E. faecalis* is also associated with community acquired endocarditis. Characteristic signs of infection include fever or a new murmur. Typical stigmata of endocarditis like petechiae, osler spots are rare and occur with sub-acute infections. Genitourinary infection or instrumentation often precedes the onset of enterococcal endocarditis. In published series of

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*Enterococci: An Important Nosocomial Pathogen DOI: http://dx.doi.org/10.5772/intechopen.90550*

coccal endocarditis remains around 20%.

**10. Gastrointestinal infections (GI)**

of colon cancers are caused due to genetic mutations.

**11. Central nervous system infections (CNS)**

**12. Skin and skin structure infections (SSSE)**

increased protein levels.

capsular polysaccharide.

**9. Intra-abdominal and pelvic infections**

enterococcal endocarditis men often outnumber women and mostly it occurred in elderly individuals. In the current therapeutic regimes, the mortality rate of entero-

VRE has been isolated from intra-abdominal and pelvic infections. The usual infections include abscesses wounds or peritonitis. Often it is a part of polymicrobial infection with Gram negative or anaerobic organisms. Usually infecting strains originate from patients intestinal flora and cause intra-abdominal infection. Enterococci are able to cause monomicrobial peritonitis infections particularly in

GI related enterococcal infections are opportunistic infections particularly occurring during colorectal surgery and colorectal cancer. Pre-colonization with VRE in patients can result in bacteremia following antibiotic induced disruption of gut microbiota [37]. Reg IIIy, a c type lectin is secreted by intestinal epithelial and paneth cells that removes Gram positive bacteria from the gut. Antibiotic treatment causes Reg IIIy down-regulation [38]. Therapeutic strategies have been devised to prevent intestinal colonization of resistant enterococci, introducing probiotic *E. faecalis* pheromone induced killing of drug resistant *E. faecalis* reactivating Reg IIIy introducing obligate anaerobic commensal bacteria containing *Barnesiella* species which prevents *E. faecium* gut colonization and bacteremia [39]. High collagenase producing *E. faecalis* strains have been found to be associated with colorectal anastomotic leak by activating tissue matrix metalloproteinase 9 that cleaves host extracellular matrix [40]. Enterococci produce menaquinone and extracellular superoxide in intestine. This results in high oxidative stress which is linked with colorectal cancer as high genomic instability of intestinal tumor cells as around 80%

Although CNS infections have been reported rarely with VRE but occur in elderly patients having underlying health issues like malignancies, pulmonary and cardiac complications [41]. In them VRE *faecium* is reported at 82% and less so of VRE *faecalis.* These infections present as fever, mental disorientation, focal CNS deficits and petechial rash. CSF investigations show pleocytosis, low glucose and

Enterococci are part of polymicrobial infections which are found to be associated with SSSE [42]. Enterococci are frequently isolated from diabetic foot ulcers and 2–5% of patients undergoing inpatient surgery. In studies using animal models it has been seen that *E. faecalis* capsular polysaccharide in SSSI predominantly is related to the persistence of the organism. A gene cpsI encodes the carbohydrate for

patients undergoing chronic peritoneal dialysis or liver cirrhosis.

*Pathogenic Bacteria*

**7. Bacteremia**

enterococcal causing pyelonephritis [33].

sensitive (VSE) bacteremia [18].

**8. Infective endocarditis**

force and even antibiotics. These enterococci utilize fibrinogen formed on catheter surface and form resistant biofilms*. E. faecalis* attachment in biofilm formation seen in vitro is partially inhibited by uropathogenic *E. coli* (UPEC) but biofilm formation by *K. pneumoniae* or UPEC are not affected by *E. faecalis* but *E. faecalis* increased *E. coli* biofilm mass accumulation and it has been seen that co-culture of an *E. faecium* probiotic strain with enteropathogenic *E. coli* increased the antibiotic sensitivity of *E. coli* to aminoglycosides, B-lactams and quinolones [33]. Biofilm formation confers the organism resistance to phagocytosis and antimicrobial agents. UTI by *E. faecalis* is mediated by virulence factors of the genes esp., srtC, ebp A, ebpC, ace, epaB, msrA, msr B, sigV, efbA, and grvR/etaR. *E. faecium* also displays similar genes related to virulence. Both *E. faecalis* and *E. faecium* isolated from nosocomial UTIs show kidney tropism. It is important to study factors in

There is a high prevalence of blood stream infections caused by Gram-positive bacteria and 45% are caused by Enterococci. Bacteremia is a common manifestation of vancomycin resistant Enterococci. Due to use of intravascular and urinary catheters these nosocomial infections are acquired. *E. faecium* in the blood stream is associated with increased mortality due to high levels of resistance. Risk factors identified with VRE bacteremia include intestinal colonization, long term antibiotic use, severity of illness, bone marrow transplant, hematologic malignancy, indwelling urinary catheters, corticosteroid treatment, chemotherapy and parenteral nutrition [34]. Studies have shown that bacteremia caused by vancomycin resistant Enterococci strains carry higher mortality rates (2.5-fold increase) as compared to bacteremia caused by vancomycin sensitive strains. In one such study the prognosis of VRE bacteremia was not much changed even with the availability of antimicrobial agents with greater potency. *E. faecalis* sigma factor Sig V that regulates gene expression in response to stress conditions has been implicated in enterococci survival and colonization in systemic infection. Absence of sig V in systemic infection in mice resulted in attenuation of bacterial translocation reducing colonization of kidney and liver. Virulence factors like Bgs A and Bgs B have also been implicated in colonization of endocarditic lesions and bacteremia. BgsA and Bgs B are now being used to treat enterococcal infections by using them as drug targets [35]. Similarly gene Asr has been implicated in *E. faecium* pathogenesis in systemic infections. Nosocomial enterococcal bacteremia have been associated with urinary catheters, intra-abdominal, burn wound, pelvic, biliary and bone sources. VRE bacteremia results in 2.5-fold increase in mortality as compared to vancomycin

Enterococci are the second most cause of infective endocarditis. Endocarditis caused by VRE faecalis causes GI or GU manipulation, damaged mitral or aortic valve infections, liver transplantation whereas VRE faecium endocarditis is associated with infection of tricuspid valve [36]*. E. faecalis* is also associated with community acquired endocarditis. Characteristic signs of infection include fever or a new murmur. Typical stigmata of endocarditis like petechiae, osler spots are rare and occur with sub-acute infections. Genitourinary infection or instrumentation often precedes the onset of enterococcal endocarditis. In published series of

**86**

enterococcal endocarditis men often outnumber women and mostly it occurred in elderly individuals. In the current therapeutic regimes, the mortality rate of enterococcal endocarditis remains around 20%.
