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Enterococci have emerged as an upgrading important cause of
nosocomial infections in the last decades. They are Gram-positive cocci that often appears in pairs (diplococci) or short chains, Enterococcus species were formerly
classified in the genus streptococcus, e.g. S. fecalis, but DNA-rRNA homology
studies show that they differ from the streptococci and now they are placed in
separate  genus Enterococcus. They are
primarily commensal residents of the intestine, though some also cause urinary
and other infections.1

only 12 species of enterococci
causing infection, The most common species causing outbreaks in hospitals
are  E. faecalis(90-95%) and E. faecium(5-10%.) 2

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Though, earlier it was a
harmless commensal of GIT. But during the past decade, there has been a
worldwide trend in increasing occurrence of nosocomial infection (hospital
acquired).as well as bacteremia, endocarditis, UTI’s, SSI and other device
associated infections. Enterococci were reported as the second most common
cause of nosocomial infections.3 Urinary tract infections (UTIs) are
most frequent infections caused by enterococci sp. intra abdominal and intra
pelvic abscesses or post surgery wound infections have been generally the
second most frequent cause of enterococcal infections.4


Numerous virulence factors are thought to
provide of E. faecalis infections. A plasmid-encoded hemolysin called the cytolysin, is major important for
pathogenesis of infection in animal models and the combination of cytolysin
with high-level gentamicin resistance is associated with a five-fold
enhance in risk of death in human bacteremia patients.5,6.A plasmid-encoded factor called aggregation substance is also
significant for virulence in animal models of infection.7

presumed virulence determinant is the enterococcal surface protein gene esp
positioned on a pathogenicity island (PAI) in both E. faecalis and E. faecium.8,
9 Esp proteins are expressed in both species at the surface of the
bacterium. They restrain an N-terminal signal sequence and domain of an
N-terminal followed by three repeat domains elected A, B, and C, with the
number of repeats varying among strains.8, 10 The C-terminal end of
Esp consists of a (Y/F)PxTG motif, which is most probably responsible for
cell-wall anchoring.

In E. faecalis, Esp has been recognized
as a alleged virulence factor involved in colonization of the urinary tract.11
Contradictory results have been reported about the role of E. faecalis Esp in
biofilm development and ranging from important loss of biofilm formation in E.
faecalis Esp-deficient mutants to no evident effect.12 Also, no
association was found in different studies between the presence or absence of
esp in clinical isolates and biofilm formation.13


Previously vancomycin was the reserved
drug for the recent enterococcal infection but the appearance of vancomycin
resistance strains has been increasing reported. Although, Enterococci are normally present in gastro
intestinal tract. So it readily passes through faecal matter. Those patients
are treating with Glycopeptide like antibiotics are more at risk
of picking up VRE.  The most likely modes
of transmission proximity
from patient to patient are
colonized with VRE especially those with diarrhoea.
Either by direct contact through transient carriage of VRE on the hands of
personnel or indirectly by infected environmental surfaces and other equipment
for patient care. Most infections with these micro-organisms are aspectable to
the patient’s own flora. VRE are capable of prolonged survival on hands, gloves
and environmental surfaces such as over-bed tables and call bells, door handles
and stethoscopes.14 Another Risk factors for bacteremia with VRE
include hemodialysis, receipt of corticosteroids, anti-neoplastic agents or
total parenteral nutrition, surgery, severity of illness, indwelling bladder
catheters, antimicrobial administration, neutropenia and mucositis.15


emergence and spread of vancomycin resistance as well as other glycopeptide agents like
teicoplanin among Enterococcus sp.
significantly reduces the number of treatment options. In addition, increase of
vancomycin-resistant Enterococci represents an immediate threat to public
health.16, 17 the prevalence and incidence
of VRE colonisation vary broadly among hospitals and studies have suggested
that such VRE rates are elevated among critically ill patients, particularly
those admitted to different ICUs, limiting the therapeutic options accessible.18

 Glycopeptide resistance in enterococci is
related with diverse phenotypes and their resistance to several antimicrobial
agents, whether in­trinsic of low-level penicillin resistance, also resistance
to cephalosporins and aminoglycosides or high concentrations of aminoglycosides
and acquired glyco­peptides resistance is of major concern. 19


The susceptibility of Enterococcus species easily
accomplish to genes resistance and the presence of some distinctive mechanisms
conferring resistance to antibiotics like glycopeptides and aminoglycosides
have cruelly deficient the choices available for treating severe infections due
to these organisms. The emergence of multi-drug resistant enterococci has lead
to a scenario which is almost as bad as the pre antibiotic era. Since many of
these multi-drug resistant strains have developed resistance to almost all
accessible antibiotics. According to the National Nosocomial Infections
Surveillance (NNIS) data resistance
of Vancomycin among Enterococcus sp.
is a major threat in most of the western world, especially in the United
States. 20


evolution of multi and vancomycin-resistant variants which do not respond to
the standard antibiotic regimes are posing a great challenge. E. Faecium considered as the source of acquired vancomycin resistance is in
the species. Amongst the eight types of acquired vancomycin resistance
genotypes vanA-vanN which are known in Enterococci, the worldwide most prevalent
genotype is VanA and followed by vanB.21VanB type resistance is
expressed by resistance to vancomycin and susceptibility to glycopeptides like
teicoplanin. This means that the MICs against vancomycin are several dilution
steps lower in VanB strains (4–64?mg/L) than VanA (commonly 16–512?mg/L). This
may make difficult performance of analytical assays, assessing the resistance
of phenotype and predicting the corresponding genotype .22    


For the treatment of VRE so many drugs are available in market but
it’s too much costly.  Linezolid, Daptomycin are commonly choice able drug against VRE.
Until recent times, the VRE strains were found sensitive to Linezolid.
Resistance to Linezolid is gradually developing, pretense several questions on
the virulence factors and their survival mechanisms.23 in this
condition, Quinupristin or dalfopristin both are selective drug on VRE.


The present study was undertaken in
MMIMSR hospital to detect VRE in the feacal sample of ICU’s patients and
non-hospitalized individuals. Since by implementing proper infection control
practices transmission of VRE can control.




Historically, the proportion of infections due to E.
faecalis to those due to all other Enterococcus species was around 10:1. In the
recent years, there has been a developing refuse in this ratio.24 While
E. faecalis remains the main species in clinical infection, E. faecium isolates
are raising in quantity. The inclination is predominantly true for blood
isolates where the ratio of E. faecium to E. faecalis has decreased from 1:3.7
in 1996 to 1:1.9 in 1999.25This microbiologic transfer is likely to
be explained in part by the manifestation of VRE and E. faecium being the
prevailing species identified among VRE. In a judgment of NNIS (National
Nosocomial Infection Surveillance) pathogens from 1994 through 1998 and May
1999, there was a 47 per cent enhance in VRE.26

Nosocomial infection in the 1990s,
called for a reassessment of public research priorities. One of the organisms
that caused disquiet was Vancomycin Resistant Enterococcus (VRE) that was first reported in 1988 in
France.27 since then; the happened of VRE have been reported in many parts of the world. The number of
cases contaminated with VRE, Centers for Disease Control and Prevention in US,
they reported VRE has risen randomly from 99 in 1992 to 278 in 1994. The more
recent reports are both worrying as well as frightening. Studies proposition
that prolonged hospital stay and the unreasonable use of vancomycin were
significant risk factors for both VRE. Other essential factors that were allied
with the appearance of vancomycin-resistant Enterococci were renal dialysis and
or in renal failure, prior use of aminoglycoside and the use of third
generation cephalosporins. It also emphasized on the significance of
transmission for VRE in clinical samples. VRE is known to cause major mortality and
morbidity. Enterococcus or VRE both are bacterial strains of the genus
Enterococcus that are resistant to the Vancomycin antibiotic. To become VRE, VSE
normally achieve new DNA in the form of plasmids or convey on which encode
genes that present VR. This acquired VR is illustrious from the lower-level,
natural Vancomycin resistance of certain enterococcal sp. including E.
casseliflavus and E. gallinarum. High-level resistance of Vancomycin E. faecium
and E. faecalis clinical isolates were first recognized in Europe in the late
1980s. Since then, VRE have been connected with out-breaks of nosocomial
infections all over the world. In US, the CDC and Prevention National
Healthcare Safety Network reported that Vancomycin-resistant E. faecium was
allied with 4% of healthcare associated infections from January 2006 to October
2007. VRE can be accepted by healthy people who have approach into contact with
the bacteria. The most likely position where such contact can occur is in a

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