Enterococcus faecalis
Enterococcus faecalis
Enterococcus faecalis is a Gram-positive bacterium that is commonly found in the human gastrointestinal tract. While usually a harmless commensal, it can act as an opportunistic pathogen, causing a range of infections, particularly in hospitalized patients. Understanding its microbiology and clinical impact is essential for effective diagnosis and treatment.
Introduction
- Definition and general characteristics: Enterococcus faecalis is a facultatively anaerobic, Gram-positive cocci that can exist as a commensal organism in the gut but may cause opportunistic infections in immunocompromised individuals.
- Historical background and discovery: E. faecalis was first identified in the late 19th century and initially classified as part of the Streptococcus genus before being reclassified under Enterococcus based on genetic and phenotypic characteristics.
- Clinical relevance and importance in human health: E. faecalis is a leading cause of hospital-acquired infections, including urinary tract infections, bacteremia, and endocarditis. Its ability to acquire antibiotic resistance, particularly vancomycin resistance, makes it a significant clinical concern.
Microbiological Characteristics
Taxonomy and Classification
- Genus and species classification: Enterococcus faecalis belongs to the genus Enterococcus within the family Enterococcaceae.
- Phylogenetic relationships: E. faecalis is closely related to other Enterococcus species such as E. faecium, but differs in virulence factors and antibiotic susceptibility.
Morphology and Structure
- Gram-positive cocci arrangement: Cells are typically found in pairs or short chains under microscopic examination.
- Cell wall composition and surface structures: The bacterium has a thick peptidoglycan cell wall containing teichoic acids and surface proteins that contribute to adhesion and virulence.
Cultural Characteristics
- Growth conditions and media: E. faecalis grows well under aerobic and anaerobic conditions on standard media such as blood agar and nutrient agar.
- Colony morphology: Colonies are typically small, greyish, and may exhibit alpha or gamma hemolysis on blood agar.
- Biochemical properties: E. faecalis is catalase-negative, exhibits bile-esculin hydrolysis, and can grow in high salt concentrations (6.5% NaCl) and at elevated temperatures (45°C).
Virulence Factors
- Adhesins and surface proteins: Surface proteins such as aggregation substance (AS) and enterococcal surface protein (Esp) facilitate adherence to host tissues and medical devices.
- Biofilm formation: E. faecalis can form biofilms on indwelling medical devices, contributing to persistent infections and resistance to antimicrobial therapy.
- Enzymes: Enzymes like gelatinase and cytolysin enhance tissue invasion, promote cell lysis, and increase virulence.
- Resistance to host defenses: The bacterium can evade immune responses through mechanisms such as capsule formation and resistance to phagocytosis.
Pathogenesis
- Mechanisms of colonization and infection: E. faecalis adheres to epithelial surfaces, invades tissues, and survives under harsh environmental conditions, establishing infection.
- Host immune response: Infection triggers innate immune responses including neutrophil recruitment and cytokine production, but E. faecalis can resist killing and persist within host tissues.
- Interaction with other microorganisms: E. faecalis can co-exist with other pathogens, enhancing virulence through synergistic interactions in polymicrobial infections.
Clinical Manifestations
- Urinary tract infections: E. faecalis is a common cause of catheter-associated urinary tract infections, presenting with dysuria, frequency, and sometimes hematuria.
- Endocarditis: The bacterium can infect heart valves, leading to subacute bacterial endocarditis, especially in patients with pre-existing valvular disease.
- Wound and intra-abdominal infections: E. faecalis can cause surgical site infections, abscesses, and peritonitis following abdominal surgery or trauma.
- Sepsis and bacteremia: In immunocompromised patients, E. faecalis can enter the bloodstream, resulting in systemic inflammatory response and septicemia.
- Other opportunistic infections: Rarely, the bacterium can cause infections in the central nervous system, respiratory tract, and ocular tissues.
Diagnosis
- Specimen collection and laboratory processing: Proper collection of urine, blood, wound swabs, or tissue samples is critical for accurate detection.
- Culture-based identification: Isolation on selective media such as bile-esculin agar and observation of colony morphology help identify E. faecalis.
- Molecular methods: Polymerase chain reaction (PCR), sequencing, and other molecular techniques provide rapid and specific identification.
- Antimicrobial susceptibility testing: Determining susceptibility to ampicillin, vancomycin, and other antibiotics guides effective treatment and identifies resistant strains.
Treatment and Management
- Antibiotic therapy: Ampicillin is the preferred first-line treatment for susceptible strains, while vancomycin or linezolid is used for resistant infections.
- Management of vancomycin-resistant Enterococcus (VRE): Treatment options include linezolid, daptomycin, and tigecycline, often guided by susceptibility testing.
- Supportive care and infection control: Management includes removal of infected catheters or devices, monitoring for systemic complications, and supportive measures for critically ill patients.
Prevention and Infection Control
- Hospital infection control measures: Isolation of infected patients and adherence to contact precautions prevent nosocomial transmission.
- Hand hygiene and environmental cleaning: Proper handwashing, use of gloves, and routine cleaning of surfaces and medical equipment reduce the risk of infection.
- Antibiotic stewardship programs: Judicious use of antibiotics minimizes the development of resistance and limits the spread of resistant E. faecalis strains.
Recent Advances and Research Directions
- Novel antimicrobial agents and therapies: Research is focused on developing new antibiotics, bacteriophage therapy, and antimicrobial peptides to combat resistant E. faecalis strains.
- Vaccine development efforts: Studies are exploring vaccines targeting surface proteins and virulence factors to prevent infections in high-risk populations.
- Genomic studies and resistance mechanisms: Whole-genome sequencing and molecular analysis are identifying genetic determinants of virulence and antibiotic resistance, aiding in surveillance and therapeutic strategies.
References
- Lebreton F, Willems RJL, Gilmore MS. Enterococcus diversity, origins in nature, and gut colonization. In: Gilmore MS, Clewell DB, Ike Y, Shankar N, editors. Enterococci: From Commensals to Leading Causes of Drug Resistant Infection. Boston: Massachusetts Eye and Ear Infirmary; 2014.
- Huycke MM, Sahm DF, Gilmore MS. Enterococcal infections, epidemiology, and implications for treatment. In: Murray PR, Baron EJ, Jorgensen JH, Landry ML, Pfaller MA, editors. Manual of Clinical Microbiology. 10th ed. Washington, DC: ASM Press; 2011. p. 356-368.
- Franz CMAP, van Belkum MJ, Holzapfel WH, Abriouel H, Gálvez A, Mayo B. Enterococci as probiotics and their implications in food safety. Int J Food Microbiol. 2011;151(2):125-140.
- Hollenbeck BL, Rice LB. Intrinsic and acquired resistance mechanisms in enterococcus. Virulence. 2012;3(5):421-433.
- O’Driscoll T, Crank CW. Vancomycin-resistant enterococcal infections: Epidemiology, clinical manifestations, and optimal management. Infect Drug Resist. 2015;8:217-230.
- Gordon DM, Murray BE. Enterococcus. In: Mandell, Douglas, and Bennett’s Principles and Practice of Infectious Diseases. 9th ed. Philadelphia: Elsevier; 2020. p. 2667-2680.
- Fisher K, Phillips C. The ecology, epidemiology and virulence of Enterococcus. Microbiology. 2009;155(Pt 6):1749-1757.
- Ruoff KL. Enterococcus. In: Baron S, editor. Medical Microbiology. 4th edition. Galveston: University of Texas Medical Branch; 1996.
- Shankar N, Baghdayan AS, Gilmore MS. Modulation of virulence in Enterococcus faecalis: Impact on pathogenesis. Curr Opin Microbiol. 2002;5(1):37-42.
- Ubeda C, Taur Y, Jenq RR, Equinda MJ, Son T, Samstein M, et al. Vancomycin-resistant Enterococcus domination of intestinal microbiota is enabled by antibiotic treatment in mice and precedes bloodstream invasion in humans. J Clin Invest. 2010;120(12):4332-4341.