Fusidic Acid Resistance among Staphylococcus aureus Causing Community Acquired Skin and Soft Tissue Infections

Safaa Sobhy Mahmoud Abo Elnour


SUMMARY AND CONCLUSION A ntibiotic resistance is becoming an increasing problem in both community and hospital acquired infections. Multidrug resistant Staphylococcus aureus (S. aureus), in particular is a major human pathogen and is responsible for many types of infections. It causes the vast majority of skin and soft tissue infections (SSTIs) in humans of varying severity, ranging from mild to life-threatening infections such as necrotizing fasciitis. SSTIs involve microbial invasion of the skin and underlying soft tissues. They have variable presentations, etiologies and severities. Protocols for management of SSTIs differ as regard severity of infection and according to presence of pus. Lines of treatment include oral antibiotics and intravenous antibiotics in mild and moderate non purulent infections. Surgical consultation is mandatory to rule out necrotizing process, empiric antibiotics and defined antibiotics in severe non purulent forms. Incision and drainage with culture and sensitivity and defined antibiotics are the main lines of treatment of purulent SSTIs. Fusidic acid (FA) is an antibiotic with effective antimicrobial activity against S. aureus infections that has been widely used over the last 20 years. It binds to elongation factor G (EF-G) preventing its release from the ribosome which results in stalling protein synthesis. Topical preparations containing FA are widely used in some regions for multiple dermatological disorders especially infected atopic eczema and impetigo. The increased usage of monotherapy FA topical preparations has been strongly associated with emergence of FA resistance among both methicillin sensitive and methicillin resistant S. aureus (MRSA). Two major mechanisms for FA resistance have been reported. One of them is alteration of the drug target site EF-G due to mutations in fusA gene encoding it or fusE gene encoding ribosome protein L6. The other mechanism is protection of drug target site by the FusB-family proteins. The FusB proteins bind to EF-G on the ribosome to prevent binding of FA, allowing translation to continue. These FusB-family proteins are encoded by fusB, fusC, fusD or fusF gene. The current study aimed to detect FA resistance among S. aureus either methicillin sensitive or MRSA causing community acquired (CA) SSTIs isolated from 75 patients presenting to the outpatient clinic of Dermatology Department, Ain Shams University Hospitals from October 2015 to April 2016. Acquired FA resistance genes were detected using Polymerase chain reaction (PCR). Pus or skin swabs were collected and S. aureus was isolated and identified by convential bacteriological methods.

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Other Titles مقاومة حمض الفيوسيديك في المكورات العنقودية الذهبية المسببه للعدوي الجلدية المكتسبة من المجتمع
Issue Date 2016
URI http://research.asu.edu.eg/handle/12345678/2740

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