Emergence And Dissemination Of Antimicrobial Resistance

The resistance pathways that have been discussed are not necessarily new mechanisms that have recently evolved among bacteria. By definition, antibiotics

  1. Emergence of "new" genes (e.g., methicillin-resistant staphylococci, vancomycin-resistant enterococci)
  2. Spread of "old" genes to new hosts (e.g., penicillin-resistant Neisseria gonorrhoeae)
  3. Mutations of "old" genes resulting in more potent resistance (e.g., beta-lactamase-mediated resistance to advanced cephalosporins in Escherichia coli and Klebsiella spp.)
  4. Emergence of intrinsically resistant opportunistic bacteria (e.g., Stenotrophomonas maltophilia)

Figure 11-11 Factors contributing to the emergence and dissemination of antimicrobial resistance among bacteria.

originate from microorganisms. Therefore, antibiotic resistance mechanisms always have been part of the evolution of bacteria as a means of survival among antibiotic-producing competitors. However, with the introduction of antibiotics into medical practice, clinically relevant bacteria have had to adopt resistance mechanisms as part of their survival strategy. With our use of antimicrobial agents, a survival of the fittest strategy has been used by bacteria to adapt to the pressures of antimicrobial attack (Figure 11-11).

All bacterial resistance strategies are encoded by one or more genes, and these resistance genes are readily shared between strains of the same species, between species of different genera, and even between more distantly related bacteria. When a resistance mechanism arises, either by mutation or gene transfer, in a particular bacterial strain or species, it is possible for this mechanism to then be passed on to other organisms using commonly described paths of genetic communication (see Figure 2-10). Therefore, resistance may spread to a wide variety of clinically important bacteria, and any single organism can acquire multiple genes and become resistant to the full spectrum of available antimicrobial agents. For example, there already exist strains of enterococci and Pseudomonas aeruginosa for which few effective therapeutic choices currently exist. Alternatively, multiple resistance may be mediated by a gene that encodes for a single very potent resistance mechanism. One such example is the mecA gene that encodes staphylococcal resistance to methicQlin and to all other beta-lactams currently available for use against these organisms, leaving vancomycin as the single available and effective cell wall-inhibiting agent.

In summary, antibiotic use coupled with the formidable repertoire bacteria have for thwarting antimicrobial activity, and their ability to genetically share these strategies, drives the ongoing process of resistance emergence and dissemination {see Figure 11-11). This has been manifested by die emergence of new genes of unknown origin {e.g., methicillin-resistant staphylococci and vancomycin-resistant enterococci), the movement of old genes into new bacterial hosts (e.g., penicillin-resistant N. gonorrhoeae), mutations in familiar resistance genes that result in greater potency (e.g., beta-lactamase-mediated resistance to cephalosporins in Escherichia coli), and the emergence of new pathogens whose most evident virulence factor is-intrinsic or natural resistance to many of the antimicrobial agents used in the hospital setting (e,g„ Stenotrophomonas maltophilia).

The ongoing nature of resistance emergence and dissemination dictates that reliable laboratory procedures be used to detect resistance as an aid to managing the infected patient and as a means for monitoring changing resistance trends among clinically relevant bacteria.

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Bacterial Vaginosis Facts

Bacterial Vaginosis Facts

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