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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

  1. 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.
  2. 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.
  3. 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.
  4. Hollenbeck BL, Rice LB. Intrinsic and acquired resistance mechanisms in enterococcus. Virulence. 2012;3(5):421-433.
  5. O’Driscoll T, Crank CW. Vancomycin-resistant enterococcal infections: Epidemiology, clinical manifestations, and optimal management. Infect Drug Resist. 2015;8:217-230.
  6. 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.
  7. Fisher K, Phillips C. The ecology, epidemiology and virulence of Enterococcus. Microbiology. 2009;155(Pt 6):1749-1757.
  8. Ruoff KL. Enterococcus. In: Baron S, editor. Medical Microbiology. 4th edition. Galveston: University of Texas Medical Branch; 1996.
  9. Shankar N, Baghdayan AS, Gilmore MS. Modulation of virulence in Enterococcus faecalis: Impact on pathogenesis. Curr Opin Microbiol. 2002;5(1):37-42.
  10. 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.
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