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. 11 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 1. Mundy LM, Sahm DF, Gilmore M. Relationships between Enterococcal virulence and antimicrobial resistance. Clin. Microbiol.Rev.2000; 13(4): 513 – 522. allowed them a cumulative advantage for further acquisition of genes encoding high level resistance 2. Barbara E Murray. The Life and times of Enterococcus. Clin. Microbiol.Rev.1990; 3(1): 46 – 65. to aminoglycosides, pencillins, tetracycline, chloramphenicol, and now vancomycin [1]. This 3. Guven Kayaoglu, Dag Orstavik. Virulence factors of Enterococcus faecalis: relationship to endodontic disease. 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Fusum Tanriverdi, Timur Esener, Osman Erganis, Sema Belli. An invitro test model for investigationof disinfection of dentinal tubules infected with Enterococcus faecalis. Braz Dent J. 1997; 8(2): 67 – 72. chlorhexidine is very effective against Enterococcus faecalis [8, 9]. But the study by Orstavik D, Haapaasalo M concluded that iodine-potassium 8. Schafer E Bossmann K. Antimicrobial efficacy of 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 9. Basarani B, Tjaderhane L, Santos JM, Pascon E, Grad H, Lawrence HP, Friedman S. Efficacy of Chlorhexidine and Calcium hydroxide containing medicaments against Enterococcus faecalis in vitro. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2003; 96 (5): 618 – 24. 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