Abstract
Background. Small colony variants have been implicated as the cause of several chronic disease states unmanageable by antibiotic therapy. Thus, this review evaluates the mechanisms employed by this subpopulation in the propagation of nosocomial infections involving the staphylococcal species. Furthermore, we propose several hypotheses for the evolutionary role this phenotype may play in clinical settings.
Results. Research suggests that a combined effort of certain auxotrophies contributes to a reduced metabolic rate within small colony variant bacteria. This minimizes the effect of antibiotics used against them and allows this phenotype to endure as an intracellular infection. Additionally, numerous studies have suggested that perhaps these variants alter the mechanisms of the immune system that are normally fashioned against such invasive pathogens. Studies have shown that although these variants possess reduced virulence factors compared with parental strains, they exhibit an increased ability to attach and colonize intracellularly in the host cells, making eradication difficult.
Conclusions. The formation of a small colony variant phenotype has been found to be a vital mode of existence for nosocomial bacteria, as it offers numerous survival options without expending valuable metabolic resources while sustaining severe chronic infections. It is suggested that intracellular survivability is the major role played by this variant. There is a need to develop clinical techniques that will be sensitive for the rapid detection and diagnosis of these variant populations. Ultimately, understanding the survival mechanisms used by these variants is imperative for the administration of suitable treatment regimens.