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Characterization of clinical Enterococcus faecalis small-colony variants
Nele Wellinghausen1, Indranil Chatterjee, Anja Berger
1Institute of Medical Microbiology and Hygiene, University Hospital of Ulm, Ulm, Germany. nele.wellinghausen@labor-gaertner.de
Journal of Clinical Microbiology
|July 17, 2009
Summary
Enterococcus faecalis small-colony variants (SCVs) cause chronic endocarditis by altering their cell structure and metabolism. These SCVs survive better in low-oxygen environments, contributing to persistent infections.
Area of Science:
- Microbiology
- Infectious Diseases
- Cell Biology
Background:
- Chronic aortic valve endocarditis can be caused by Enterococcus faecalis.
- Enterococcus faecalis can exhibit small-colony variants (SCVs) with distinct phenotypes.
Observation:
- Enterococcus faecalis SCVs displayed heterogeneous cell morphology, aberrant shapes, and altered cell division with thick cell walls.
- SCVs showed excessive intercellular substance production and "ghost" cells.
- SCVs exhibited an extended lag phase and delayed stationary phase entry.
Findings:
- SCVs demonstrated impaired growth and viability under aerobic conditions compared to microaerobic conditions.
- Metabolite analysis revealed SCVs produced lactate under microaerobic but not aerobic conditions, indicating induced fermentative metabolism.
- Structural and metabolic alterations in SCVs facilitate survival in microaerobic environments.
Implications:
- Understanding SCV pathophysiology is crucial for developing targeted therapies for chronic Enterococcus faecalis endocarditis.
- The SCV phenotype may represent a survival strategy for bacteria in the challenging in vivo environment of endocarditis.
- Further research into SCV metabolic pathways could reveal novel therapeutic targets.
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