ENDODONTOLOGY Enterococcus Faecalis: An Endodontic ... - MedIND

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cavity, gastrointestinal tract, and vaginal vault [1]. Enterococci have been recognized as being potentially pathogenic for humans since the turn of the century [2].
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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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 treatment, an increased prevalence of bacteria 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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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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iodide appeared more potent irrigant than sodium hypochlorite or chlorhexidine [10]. While 2-5

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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 13