Microorganism-mediated resistance refers to antimicrobial resistance that is due to genetically encoded traits of the microorganism and is the type of resistance that in vitro susceptibility testing methods are targeted to detect (see Chapter 12). Organism-based resistance can be divided into two subcategories: intrinsic or inherent resistance, and acquired resistance.
Antimicrobial resistance resulting from the normal genetic, structural, or physiologic state of a microorganism is referred to as intrinsic resistance. Such resistance is considered to be a natural and consistendy inherited charaderistic that is associated with the vast majority of strains that constitute a particular bacterial group, genus, or spedes. Therefore, this is predictable resistance so that once the identity of the organism is known, so are certain aspects of its antimicrobial resistance profile. Box 11-2 lists common examples of intrinsic resistance and the underlying reason for the resistance. Intrinsic resistance profiles are useful for determining which antimicrobial agents should be induded in the battery of drugs that will be tested against specific types of organisms. For example, referring to the information given in Box 11-2, aztreo-nam would not be induded in antibiotic batteries tested against gram-positive coco. Similarly, vancomycin would not be routinely tested against gram-negative bacilli. As discussed in Chapter 7, intrinsic resistance profiles are also useful markers to aid in the identification of certain bacteria or bacterial groups.
Antibiotic resistance that results from altered cellular physiology and structure caused by changes in a microorganism's usual genetic makeup is known as acquired resistance. Unlike intrinsic resistance, acquired resistance may be a trait assodated with only some strains of a particular organism group or spedes, but not others. Therefore, the presence of this type of resistance in any clinical isolate is unpredictable, and this unpredictability is the primary reason why laboratory methods to detect resistance are necessary.
Because acquired resistance mechanisms are all genetically encoded, the methods for acquisition basically are those that allow for gene change or exchange. Therefore, resistance may be acquired by:
BOX 11-2 Examples of Intrinsic Resistance to Antibacterial Agents inca ibic bacteria vs. aminoglycosides inca
Mechanism ibic bacteria vs. aminoglycosides
Gram-positive bacteria vs. aztreonam (a beta-lactam)
Gram-negative bacteria vs. vancomycin
Pseudomonas aenjginosa vs. sulfonamides, trimethoprim, tetracycline, or chloramphenicol Klebsiella spp. vs. ampicillin (a beta-lactam) targets
Aerobic bacteria vs. metronidazole Enterococci vs. aminoglycosides Enterococci vs. all cephalosporin antibiotics Lactobacilli and Leuconostoc vs. vancomycin
Stenotrophomonas maltophilia vs. imipenem (a beta-lactam)
Lack of oxidative metabolism to drive uptake of aminoglycosides Lack of penicillin-binding proteins (PBPs) that bind and are inhibited by this beta-lactam antibiotic Lack of uptake resulting from inability of vancomycin to penetrate outer membrane
Lack of uptake resulting from inability of antibiotics to achieve effective intracellular concentrations Production of enzymes (beta-lactamases) that destroy ampicillin before the drug can reach the PBP Inability to anaerabically reduce drug to its active form Lack of sufficient oxidative metabolism to drive uptake of aminoglycosides Lack of PBPs that effectively bind and are inhibited by these beta-lactam Lack of appropriate cell wall precursor target to allow vancomycin to bind and inhibit cell wall synthesis Production of enzymes (beta-lactamases) that destroy imipenem before the drug can reach the PBP targets
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