The development of antimicrobial resistance in staphylococci

Abstract

Staphylococci are among the most important aetiological agents of both community- and hospital-acquired infections. Staphylococcus aureus isolates resistant to penicillin because they produced beta-lactamase were isolated soon after the introduction of penicillin as a therapeutic agent. The production of beta-lactamase was mediated by a plasmid. The incidence of penicillin resistance in S. aureus increased during the succeeding decades until most clinical isolates were resistant to penicillin. During the 1940s and 1950s resistance to other antimicrobial agents was also demonstrated, usually in combination with penicillin resistance, thus creating multi-resistant strains. Methicillin, a penicillin that was essentially resistant to staphylococcal beta-lactamase, was introduced into clinical use in the early 1960s and this alleviated much of the problem of antimicrobial resistance in S. aureus, but methicillin-resistant strains were soon isolated. Although methicillin-resistant staphylococci had been a nosocomial problem in Europe in the 1960s and early-1970s, it was not until the mid-1970s that they became a problem in the United States. Since then the incidence of methicillin-resistant S. aureus has steadily increased. The methicillin-resistant S. aureus strains are usually multi-resistant including the beta-lactams and one or more of the following: aminoglycosides, macrolides, lincosamides, tetracyclines (usually not minocycline), and chloramphenicol. The methicillin-resistant S. aureus are generally susceptible to vancomycin, teicoplanin, rifampicin, coumermycin, minocycline, the quinolones, and sulphamethoxazole-trimethoprim. The coagulase-negative staphylococci are also important aetiological agents of nosocomial infections and the incidence of these infections has increased in recent years.(ABSTRACT TRUNCATED AT 250 WORDS)