Impetigo and Topical Fusidic Acid Essay
Dobie and Gray stated that for more than 35 years Fusidic acid – a narrow spectrum antibiotic derived from Fusidium coccineum has been used to treat infections from Staphylococcus aureus thus making it suitable in combination with another agent for systemic therapy in vitro. In spite of controversies and recommendations, the usage of topical fusidic acid has doubled between 1995 and 2001 with increased reports of fusidic acid resistance.
Three reasons could be attributed to the fusidic acid resistance (i) “Systemic fusidic acid can no longer be used in situations where it is clinically indicated,” (ii) Failure of topical treatment (iii) Resistance may be linked to other antibiotic resistances leading to spread of antibiotic resistance like S. aureus and MRSA (methicillin resistant S. aureus). Fusidic acid inhibits bacterial protein synthesis by binding to elongation factor G (EF-G) a bacterial protein necessary for translocation.
About two thirds of usage of fusidic acid is being done for topical treatment consisting of skin infections such as impetigo, folliculitis, erythrasma, furunculosis and infected traumatic wounds as monotherapy and atopic dermatitis in combination of glucocorticoid. Studies have shown a consistent rise in resistance to fusidic acid from 1980’s and according to a recent study 68% S. aureus isolated from children with impetigo were fusidic acid resistant on the contrary a Dutch study depicted no fusidic acid resistance. MRSA showed no fusidic acid resistance.
Resistance rates of 43% have been observed in hospitalized patients the probable reason being higher bacterial burden with underlying skin diseases thus recommending short term topical or systemic treatment with fusidic acid. In order to avoid resistance topical antibiotics should not be used systemically a condition fulfilled only by mupirocin but an important point to remember being that mupirocin is drug widely used to eradicate MRSA. Readers Views: When fusidic acid has been successfully used for 35 years to treat infections caused by S.
aureus how is it that it has become resistant from 1980’s (almost for last 26 years)? If that was the case why hasn’t its usage stopped? While the authors state that probability of infections was more in patients hospitalized due to higher bacterial burden, as a reader I have strong feelings and suspicion with regards to the hygiene and infection free environment of hospitals? If the author’s words are to be believed a healthy person is more vulnerable to infection in a hospital. In that case a person could better be treated at home.
While most evidences are shown in favor of fusidic acid resistance a Dutch study depicted contrary results, this needs to be investigated thoroughly. With limited understanding of fusidic acid resistance at genetic, epidemiological and clinical level it would be improper to draw conclusion against the usage of fusidic acid in topical or systemic treatments.
D Dobie and J Gray (2004). Fusidic acid resistance in Staphylococcus aureus – A Review. Volume 89, pp: 74-77, Arch. Dis. Child. Page retrieved on November 29, 2006 http://adc.bmj.com/cgi/reprint/89/1/74
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