The Use of Mupirocin in Controlling Methicillin-Resistant Staphylococcus aureus

Methicillin-resistant Staphylococcus aureus (MRSA) have become the bane of the hospital epidemiologist and infection control practitioner (ICP) because they necessitate countless calls to the nursing service, housekeeping department and doctors involved in the case. Even in the face of increasing information about the genetic basis of methicillinresistance, we seem to have more patients who are colonized with the problem organism and even more actual infections. Where will the problem end? What can we expect for the 1990s? I do not have the answers, but I will offer some comments on the study by Cederna and colleagues in this issue, as well as some predictions for the future. Why do we seem to have more MRSA today than in the previous decade? Some of the increase is related to changes in laboratory methods used to identify MRSA. The inclusion of 2% NaCL in virtually all of the susceptibility test media is a partial explanation, as is an increased awareness of MRSA in microbiology laboratories. Increased use of cultures in larger teaching centers may also be a reason for the increase, because there is almost a knee-jerk reaction to start vancomycin therapy when a patient has a proven or suspected staphylococcal infection, and the need to justify the use of vancomycin, I suspect, results in many nasal and other cultures that would not otherwise be obtained. Another reason for the increase in MRSA may be real; that is, the extensive use of cephalosporins. Oral cephalosporins such as cephalexin are widely used in chronic care facilities and by narcotic addicts. Parenterally administered second and third-generation cephalosporins commend a major part of the hospital antibiotic armamentarium of most internists and surgeons. Why are MRSA methicillin-resistant? The reason for MRSA is the production of a new penicillinbinding protein, PBP2a, that has a low affinity for all p-lactam antibiotics.' Certainly some MRSA are not really MRSA of the altered PBP2a type, but rather are strains in which production of P-lactamase has become constitutive at a high level so that otherwise p-lactamase stable compounds such as oxacillin (the agent used to test for MRSA) are now competitive substrates that are hydrolyzed at an appreciable enough rate to make organisms have minimum inhibitory concentrations (MICs) of 8 to 16-ug/ml. These organisms are the ones that are susceptible to ampicillin-sulbactam, amoxicillinclavulanate and imipenem.2 This is very important because these isolates are not really MRSA, and when so considered and so treated add to a hospital's cost in terms of the need for isolation of MRSA