Methicillin-resistant S. aureus (MRSA), a bacterial clinical scourge, first emerges in the United Kingdom in 1961. It was disseminated globally within a couple of years and it has remained a clinical challenge to the present. Its resistance to b-lactam antibiotics is complete, encompassing virtually all commercial antibiotics of this class (currently there is one exception). This broad resistance has come about by the acquisition of several genes that work in concert in manifesting the resistant phenotype.  This presentation will outline at the molecular level how these processes take place, starting from detection of the presence of the antibiotic in the medium, to signal transduction to the cytoplasmic side, to events within the cytoplasm that unleash expression of antibiotic-resistance determinants, and ultimately to the processes that initiate the reversal of mobilization from the resistant phenotype as the challenge of the antibiotic is withdrawn. The system is efficiently inducible, so the organism recruits these extraordinary processes only when the antibiotic is present in the milieu.

Mechanism of resistance to beta-lactam antibiotics in methicillin-resistant Staphylococcus aureus (MRSA)

243rd National Meeting (2012)

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