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Genomic analysis reveals different mechanisms of fusidic acid resistance in Staphylococcus aureus.

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Dr Kiran Godse    03 January 2018

Staphylococcus aureus skin colonization is common in patients with atopic dermatitis (AD) and is associated with risk of skin infections.

A new study published in The Journal of Antimicrobial Chemotherapy examined the prevalence of antibiotic resistance in Staphylococcus aureus (S. aureus) isolated from Danish AD patients, with a primary focus on fusidic acid resistance, and the underlying genetic mechanisms.

This study included 138 S. aureus isolates collected from lesioned skin (n = 54), non-lesioned skin (n = 27) and anterior nares (n = 57) of 71 adult AD patients. Isolates were tested for susceptibility to 17 selected antibiotics.

The results revealed that 79% of isolates were resistant to at least one of the tested antibiotics, with the most prevalent resistances being to penicillin (55%), fusidic acid (41%), and erythromycin (11%). The primary genetic mechanisms of fusidic acid resistance were carriage of fusC (57%) or mutations in fusA (38%). Furthermore, the most prevalent S. aureus lineage was ST1 (23%); while all ST1 isolates carried fusC.

Hence, it was inferred that S. aureus fusidic acid resistance, caused by either fusA mutations or fusC gene carriage, is a major concern among AD patients. It was stated that resistant S. aureus might spread from the patients to the community, indicating the need to reduce the use of fusidic acid in the treatment of AD.

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