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ENDODONTOLOGY
Enterococcus Faecalis: An Endodontic Pathogen
SUCHITRA. U *
KUNDABALA. M **
ABSTRACT
Enterococci are a frequent cause of wide variety of infections in humans. Enterococcus faecalis has been isolated
from endodontic infections like obturated root canals with chronic apical periodontitis. The organism can survive
extreme challenges. In this article, we discuss the changed taxonomy, identification characters, pathogenesis of
endodontic infections by Enterococcus faecalis and its antimicrobial resistance pattern. Knowledge about the
organism may help to prevent endodontic treatment failures attributed to this organism.
Keywords: Enterococcus faecalis, endodontic treatment, antimicrobial resistance
INTRODUCTION
Thiercelin in a paper from France published in 1899;
Enterococci are normal human commensals
the name was proposed to emphasize the intestinal
adapted to the nutrient-enriched, oxygen-depleted,
origin of this organism [2]. Enterococcus faecalis is
ecologically complex environments of the oral
a nonspore-forming, fermentative, facultatively
cavity, gastrointestinal tract, and vaginal vault [1].
anaerobic, Gram-positive coccus. Enterococcus
Enterococci have been recognized as being
faecalis cells are ovoid and 0.5 to 1 µm in diameter.
potentially pathogenic for humans since the turn of
They occur singly, in pairs, or in short chains, and
the century [2]. Enterococci now rank among the
are frequently elongated in the direction of the
top three nasocomial bacterial pathogens, and
chain. Most strains are nonhemolytic and nonmotile.
strains resistant to currently available antibiotics
Surface colonies on blood agar are circular, smooth,
pose real therapeutic difficulties. Upto 90% of
and entire. The G+C content of the DNA ranges
enterococcal infections in humans are caused by
from 37 to 40mol% [4].
Enterococcus faecalis [3]. Enterococci have been
In 1930’s Lancefield serologically classified
implicated in endodontic infections. Data from
Enterococci as group D Streptococci. In 1937,
culture studies have revealed that Enterococcus
Sherman proposed a classification scheme, in which
faecalis is occasionally isolated from primary
he recommended that the term ‘enterococcus’
endodontic infections but frequently recovered from
should be used specifically for streptococci that
treatment failures [4]. The rapid emergence of
grow at both 10 & 45ºC, at pH 9.6 and in 6.5%
antimicrobial resistance among enterococci makes
NaCl, survive at 60 ºC for 30 min and have ability
it difficult to treat the chronic infections.
to split esculin [2,5].
TAXONOMY AND IDENTIFICATION
In 1980s, based on genetic differences,
The name “enterocoque” was first used by
* Assistant Professor, Department of Microbiology, Kasturba Medical College, Light House Hill Road, Hampankatta, Mangalore, Karnataka, India 575 001.
** Department of Conservative Dentistry, Manipal College of Dental Sciences, Mangalore.
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ENDODONTOLOGY
ENTEROCOCCUS FAECALIS: AN ENDODONTIC PATHOGEN
enterococci were removed from the genus
accumulate and share extrachromosomal elements
Streptococcus and placed in their own genus,
encoding virulence traits, which help to colonize,
Enterococcus. The previously used species
compete with other bacteria, resist host defense
designations such as faecalis, faecium, durans, and
mechanisms and produce pathological changes
so forth were retained but were preceded by the
directly through production of toxins or indirectly
genus name Enterococcus in place of Streptococcus
through induction of inflammation. Upon
[5]. Enterococcus faecalis causes 80-90% of human
contamination of the root canal with the bacterium,
enterococcal infections, while Enterococcus
it colonizes the dentinal walls under stressful
faecium accounts for a majority of the remainder.
conditions like nutrient deficiency and endodontic
Other enterococcal species are infrequent causes
medicaments with the help of adhesive moieties.
of human infection [5,6].
Aggregation substance, surface carbohydrates or
fibronectin- binding moieties facilitate adherence
VIRULENCE AND PATHOGENESIS
of organism to host collagen type I and extracellular
Enterococcus faecalis has been only
matrix proteins present in the dentin. Extracellular
occasionally found in cases of primary endodontic
toxins such as cytolysin may induce tissue damage,
infections but frequently isolated or detected in
while bacteriocins like AS-48 inhibit growth of other
cases in which the endodontic therapy has failed.
organisms. While, lipoteichoic acid, superoxide
Enterococcus faecalis is the most isolated or
production, or pheromones & corresponding
detected species from oral infections, including
peptide inhibitors each may modulate local
marginal periodontitis, infected root canals, and
inflammatory process by stimulating leukocytes to
periradicular abscesses [3, 4].
release several mediators like tumor necrosis factor,
Enterococci are well adapted for survival and
interleukins, & prostaglandins and contribute to the
persistence in a variety of adverse environments. It
periradicular damage [3, 6]. The enzyme
may explain its survival in root canal infections,
hyaluronidase help in degradation of hyaluronan,
where nutrients are scarce and there are limited
present in the dentin, to dissacharides and provide
means of escape from root canal medicaments. In
energy to the organism. Gelatinase produced by the
invitro studies, Enterococcus faecalis has been
Enterococcus faecalis contributes to the bone
shown to invade dentinal tubules. It can colonize
resorption and degradation of dentin organic matrix,
root canal and survive without the support of other
thus playing an important role in the pathogenesis
bacteria [3]. It is resistant to the antimicrobial effects
of periapical inflammation.
of calcium hydroxide, probably partly due to an
ANTIMICROBIAL RESISTANCE
effective proton pump mechanism which maintains
Enterococci have displayed resistance to
optimal cytoplasmic pH levels [7]. The rapid
essentially every useful antimicrobial agent. The
emergence of antimicrobial resistance among
resistance may be intrinsic or acquired via gene
enterococci helps to shift the microbial flora in
transfer. The genes for intrinsic resistance, like other
favour of Enterococcus faecalis.
species characteristics, reside on the chromosome.
The organism has the natural ability to acquire,
Acquired resistance results from either a mutation
12
ENDODONTOLOGY
ENTEROCOCCUS FAECALIS: AN ENDODONTIC PATHOGEN
in the existing DNA or acquisition of new gene,
infections helps to develop effective strategies in
through the transfer of plasmids & transposons. The
treating the infections.
intrinsic resistance of enterococci to many
BIBILOGRAPHY
commonly used antimicrobial agents may have
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to aminoglycosides, pencillins, tetracycline,
chloramphenicol, and now vancomycin [1]. This
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Enterococcus faecalis: relationship to endodontic disease. Crit.
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allows the organism to survive in an environment
in which antimicrobial agents are used. Indeed, in
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marginal periodontitis refractory to conventional
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resistant to antibiotics may be found. The focus of
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infection is the root canal and the dentinal tubules,
which are inaccessible to the elements of the host
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Virulence of Enterococci. Clin. Microbiol.Rev.1994; 7 (4): 462
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defense system. Therefore, treatment or preventive
procedures should mainly include local, rather than
systemic means. Some studies have shown that
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chlorhexidine is very effective against Enterococcus
faecalis [8, 9]. But the study by Orstavik D,
Haapaasalo M concluded that iodine-potassium
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chloroxylenol and chlorhexidine in the treatment of infected
root canals. Am J Dent. 2001; 14: 233- 7.
iodide appeared more potent irrigant than sodium
hypochlorite or chlorhexidine [10]. While 2-5
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Lawrence HP, Friedman S. Efficacy of Chlorhexidine and
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minutes exposure of Enterococcus faecalis to MTAD
is effective in killing the organism up to 200 x
dilutions [11]. In addition, to disinfectants, physical
removal of cells of Enterococcus faecalis through
10. Orstavik D, Haapasalo M. Disinfection by endodontic
irrigants and dressings of experimentally infected dentinal
tubules. Endod Dent Traumatol. 1990 Aug; 6(4):142-9.
Mahmoud Torabinejad, Shahrokh Shabahang, Raydolfo M.
Aprecio, James D. Kettering. The Antimicrobial Effect of MTAD:
An In Vitro Investigation Journal of Endodontics. June 2003;
Vol. 29, No. 6: 400-403.
debridement of the root canal remains essential,
since remnants may sustain the inflammation.
CONCLUSION
This article has dealt with the taxonomy,
identifying characters, pathogenesis, virulence
factors and antimicrobial resistance pattern of
Enterococcus faecalis responsible for chronic
periradicular inflammation and failure of endodontic
treatment. Accurate knowledge about the pathogen
and its role in the pathogenesis of endodontic
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