Produced by the Royal College of Physicians of Edinburgh and Royal College of Physicians and Surgeons of Glasgow

Methicillin Resistant Staphylococcus Aureus (MRSA) and its clinical impact

  • Dr FXS Emmanuel, Consultant Microbiologist and Honorary Senior Lecturer, Royal Infirmary of Edinburgh, Edinburgh, Scotland


MRSA is now the most common cause of hospital-acquired infection worldwide and infection rates show no sign of abating. Dr Xavier Emmanuel reviews the evolution of MRSA, its clinical impact and efforts to control and eradicate it.

Key Points

  • MRSA is so-called because resistance was described first in relation to methicillin. MRSA is, in fact, resistant to all penicillins and cephalosporines and often to several other unrelated antibiotics.
  • Treatment is difficult. MRSA are almost always sensitive to vancomycin and the related teicoplanin. Newer agents are being introduced.
  • Rapid spread of MRSA in the 1990s was due to a few closely related MRSA strains known as epidemic or E-MRSA. MRSA is now the most common cause of hospital acquired infection worldwide.
  • Antibiotic use, prolonged hospitalisation, serious underlying illness, skin disease, frequent staff-patient contact and the use of invasive devices predispose to invasive MRSA infections.
  • General cleanliness, hand-washing and sensible antibiotic use prevent infection. Patient isolation, special nursing procedures and MRSA eradications from staff are needed occasionally.

Declaration of interests: No conflict of interests declared

Staphylococcus aureus (S. aureus) is one of the oldest known and most important of bacterial pathogens, causing a wide range of superficial and deep infections. At the dramatic beginning of the antimicrobial era, it was, like many other pyogenic bacteria, very susceptible to the sulphonamides and later to penicillin. The subsequent story of antibiotic resistance in S. aureus is a good example of the evolving interaction between a pathogenic organism and antibiotics. Clinically important resistance to penicillin was noted soon after its introduction1 and spread rapidly so that, within a decade or so, penicillin resistance in S. aureus was the rule rather than the exception. This resistance is due to the production by the organism of a beta-lactamase enzyme, which lyses the essential beta-lactam ring of penicillin. The 1960s saw the development of a number of semi-synthetic penicillins such as methicillin, nafcillin, and cloxacillin which are more stable to the action of the beta-lactamase. These new agents seemed at first to solve the problem, but their widespread use was again followed by the emergence of resistant strains, described initially in relation to methicillin.2 These strains produce a modified version of a bacterial cell-wall synthesising enzyme, which enables cell-wall synthesis and bacterial multiplication to continue uninhibited even in the presence of the beta-lactamase stable semi-synthetic penicillins. This confers resistance against all antibiotics based on the beta-lactam ring structure, including the c