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Bayston et al.describe the isolation of SCVs with low-level resistance to tri-closan, reduced coagulase production, reduced haemolyticactivity and did not detect auxotrophy. They recognize, as othershave done, the possible clinical importance of SCVs and thepotential role of triclosan in their generation. However, wewould like to urge some caution in their interpretation of theirdata and consequently on the signicance of the issues raised.A signicant difference between triclosan and other antimi-crobials known to select for SCVs (principally aminoglycosides)is that it is used topically. It is thought that SCVs are unlikely toinitiate infections, rather, once a wild-type infection has beenestablished, antibiotic treatment selects for mutation to give theSCV phenotype/form. Hence, selection of SCVs by systemicantibiotics occurs once the bacteria have broached the skin andare at the site of infection, whereas triclosan-induced SCVs willpresumably be on the skin surface. Thus, an important questionis whether these SCVs would then be capable of ever initiatingan infection in healthy individuals.Extending this logic means the triclosan-induced SCVsformed at the skin surface may be transmissible by skin–skincontact, as wild-type S. aureus. This could provide a mechanismfor them coming into contact with wounds or nding otherroutes through the epidermis. However, it would also leave themvulnerable to the current mechanisms of preventing transfer ofinfection, such as alcohol hand-washes and barrier systems suchas gloves.The association of SCVs with triclosan-impregnated polymersis possibly more worrying than selection of SCVs by topicalpreparations. For example, the use of triclosan-impregnatedsutures

the journal of antimicrobial chemotherapy/journal of antimicrobial chemotherapy

Comment on: Triclosan resistance in methicillin-resistant Staphylococcus aureus expressed as small colony variants: a novel mode of evasion of susceptibility to antiseptics