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Staphylococcus aureus small colony variants: formation and clinical impact
C von Eiff1, R A Proctor, G Peters
1Institut für Medizinische Mikrobiologie, Westfälische Wilhelms-Universität, Münster, Germany.
International Journal of Clinical Practice. Supplement
|February 24, 2001
Summary
Staphylococcus aureus small-colony variants (SCVs) are linked to persistent infections. A hemB mutant demonstrated that reduced alpha-toxin production by SCVs may shield them from antibiotics and host defenses.
Area of Science:
- Microbiology
- Infectious Diseases
- Bacterial Pathogenesis
Background:
- Small-colony variants (SCVs) of Staphylococcus aureus are slow-growing subpopulations.
- SCVs exhibit atypical characteristics, including reduced alpha-toxin and delayed coagulase activity.
- SCVs are associated with persistent and relapsing infections, particularly in chronic osteomyelitis and cystic fibrosis.
Purpose of the Study:
- To investigate the role of Staphylococcus aureus small-colony variants (SCVs) in persistent infections.
- To provide evidence linking specific genetic defects to the SCV phenotype and its clinical implications.
Main Methods:
- Characterization of S. aureus SCVs from clinical isolates.
- Generation and analysis of a defined hemB mutant exhibiting the SCV phenotype.
- Assessment of bacterial-host cell interactions, including phagocytosis and cell lysis.
Main Results:
- Studies with clinical SCV isolates suggested a link between electron transport defects and persistent infections.
- A defined hemB mutant displayed the SCV phenotype, reduced alpha-toxin production, and delayed coagulase activity.
- The hemB mutant was phagocytosed by endothelial cells but did not cause lysis due to low alpha-toxin levels.
Conclusions:
- The hemB mutation provides strong evidence for the connection between SCV phenotype and persistent infections.
- Reduced alpha-toxin production by SCVs may facilitate intracellular survival within host cells.
- Intracellular sequestration of SCVs offers a potential mechanism for evading host defenses and antibiotic treatment, explaining treatment challenges.