Abstract
Sudden increases in prevalence of antimicrobial resistance among bacteria are seen in both hospital-acquired and community-acquired infections. Examples include precipitate change in amikacin susceptibility in a hospital after years of low resistance, the abrupt increase in prevalence of β-lactamase-producing strains among gonococci isolated in one community, and rapid increase in resistance to ciprofloxacin among methicillin-resistant Staphylococcus aureus at a hospital shortly after the drug was introduced. Most dramatic are cases where organisms have abruptly become resistant to drugs that have worked clinically for decades (e.g. resistance to ampicillin in Haemophilus influenzae). Four types of mechanisms (other than laboratory artefact) for development of resistance can be postulated: introduction of resistant organisms into a previously susceptible population; acquisition of resistance by previously susceptible strains through genetic mutation or transfer of genetic material from another species or genus; emergence of a dormant resistance mechanism already present in the population; selection of resistant subpopulations of organisms. When any of these resistance mechanisms develop in a large proportion of the organisms, or in a few resistant organisms which are widely disseminated within the population, resistance can increase abruptly. It is likely that organisms will continue to use the mechanisms described here, and to develop additional ingenious ways to counter our antimicrobial weapons. Infection control personnel must rapidly uncover which mechanisms are involved so that appropriate measures (alternate drug regimens, isolation precautions, cohorting, etc.) can be instituted. Newer methods for typing of organisms can help identify which resistance mechanisms are involved in a given situation. Further study is also needed of the factors eliciting these dramatic changes; antimicrobial use is one but not the only contributor.
Published Version
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