Diverse molecular mechanisms underpinning Staphylococcus aureus small colony variants

• Published in: Trends in microbiology (Regular ed.) 2024-10
• Main Authors: Mapar, Maryam, Rydzak, Thomas, Hommes, Josefien W., Surewaard, Bas G.J., Lewis, Ian A.
• Format: Article
• Language: English
• Subjects: biofilm formation; global regulatory systems; host–pathogen interaction; metabolism; small colony variants
• ISSN: 0966-842X; 1878-4380; 1878-4380
• DOI: 10.1016/j.tim.2024.09.007

Small colony variants (SCVs) are an alternative bacterial growth form associated with chronic and recurrent infections.SCVs arise from a diverse range of mutations affecting metabolism or global regulatory systems.SCVs modulate host–pathogen dynamics through numerous molecular mechanisms.SCVs should be viewed as an ensemble of phenotypes, not as a signal phenomenon. Small colony variants (SCVs) of Staphylococcus aureus are a relatively rare but clinically significant growth morphotype. Infections with SCVs are frequently difficult to treat, inherently antibiotic-resistant, and can lead to persistent infections. Despite a long history of research, the molecular underpinnings of this morphotype and their impact on the clinical trajectory of infections remain unclear. However, a growing body of literature indicates that SCVs are caused by a diverse range of molecular factors. These recent findings suggest that SCVs should be thought of as an ensemble collection of loosely related phenotypes, and not as a single phenomenon. This review describes the diverse mechanisms currently known to contribute to SCVs and proposes an ensemble model for conceptualizing this morphotype. Small colony variants (SCVs) of Staphylococcus aureus are a relatively rare but clinically significant growth morphotype. Infections with SCVs are frequently difficult to treat, inherently antibiotic-resistant, and can lead to persistent infections. Despite a long history of research, the molecular underpinnings of this morphotype and their impact on the clinical trajectory of infections remain unclear. However, a growing body of literature indicates that SCVs are caused by a diverse range of molecular factors. These recent findings suggest that SCVs should be thought of as an ensemble collection of loosely related phenotypes, and not as a single phenomenon. This review describes the diverse mechanisms currently known to contribute to SCVs and proposes an ensemble model for conceptualizing this morphotype.