Overview

MRSA Background

The continual misuse of antibiotics has resulted in one of the most serious potential risks to public health safety (World Health Organization, 2011). The propagation of antibiotic-resistant phenotypes of infectious microorganisms is challenging the conventional wisdom of disease treatment, and requires innovative applications of genetics, biochemistry, and synthetic biology to address this looming threat.

Methicillin-resistant Staphylococcus aureus (MRSA) possesses the mecA gene which encodes for penicillin-binding-protein 2a (PBP2a). PBP2a is unaffected by the antimicrobial properties of methicillin, penicillin or other β-lactam antibiotics (Lim & Strynadka, 2002). While 20-30% of the population may possess MRSA cells on their skin at any given time (Public Health Agency of Canada, 2008), to date, the Centers for Disease Control and Prevention (2013) have over 75 000 recorded instances of MRSA infections, with many fatalities involving the elderly or immunodeficient. If β-lactam antibiotics do not successfully curb the infection of a given patient, alternative antibiotics such as tetracyclines are administered. In the case that lesions or abscesses form, invasive procedures are a last resort (CDC, 2013). These practices are ultimately not sustainable - microorganisms will inevitably also become resistant to these antibiotics (Infectious Diseases Society of America, 2011). The low profits associated with the discovery of novel antibiotics (Norwich BioScience Institutes, 2013) is creating pressure for researchers to discover infectious disease treatment mechanisms to address antibiotic resistance at a genetic level.

References

Daniel Lim, N. C. (2002). Structural basis for the bold beta lactam resistance of PBP2a from methicillin-resistant Staphylococcus aureus. Nature Structural Biology, 870-876.