Staphylococcus aureus remains a versatile and dangerous pathogen. Small-colony variants (SCVs) of S. aureus are a naturally occurring sub-population, first described nearly 100 years ago. These variants, of which there are different classes, grow slowly and have many atypical characteristics thought to be due to defective electron transport, and include minute colony forms. SCVs have been isolated from sites of infection, particularly persistent recurrent ones (e.g. in chronic osteomyelitis and cystic fibrosis), and also may arise following exposure to certain antibiotics. During infection the intraendothelial-cell milieu stimulates the formation of SCVs, which can better survive the assault of cell-mediated immunity. SCV phenotypes produce less tissue damage than normal staphylococci. Although microscopic morphology and Gram's staining of SCVs are normal, clinical microbiology laboratories may fail to detect them because of their very slow growth. The full extent of the role of S. aureus SCVs in clinical disease, and the most appropriate means of identifying such strains or testing to predict the clinical usefulness of therapeutic regimens, remains unknown. Failure to recover SCVs results in a major susceptibility reporting error, as the more resistant component of the infection will not have been reported. No controlled trials of therapy have been conducted, and, thus, optimal therapy has yet to be defined. However, SCVs are resistant to aminoglycoside antibiotics, and may be resistant to trimethoprim-sulphmethoxazole. The effectiveness of cell-wall-active antibiotics is reduced. SCVs are transmissible, and current infection control recommendations for normal S. aureus infections are appropriate.
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