Whether resistance is intrinsic or acquired, bacteria share similar pathways or strategies to effect resistance to antimicrobial agents. Of the pathways listed in Figure 11-8, those that involve enzymatic destruction or alteration of the antibiotic, decreased intracellular uptake or accumulation of drug, and altered antibiotic target are the most common. One or more of these pathway j may be expressed by a single cell to successfully avert the action of one or more antibiotics.
Bacterial resistance to beta-lactams may be mediated by enzymatic destruction of the antibiotics, altered antibiotic targets, or decreased intracellular uptake of ch drug (Table 11-3), All three pathways play an important role in clinically relevant antibacterial resistance, but bacterial destruction of beta-lactams by producing beta-lactamases is by far the most common method of resistance. As shown in Figure 11-9, beta-latfamases open the beta-lactam ring and the altered structure of the drug prohibits subsequent effective binding to PBPs so that cell wall synthesis is able to continue.
Staphylococci are the gram-positive bacteria that most commonly produce beta-lactamase; approximately 90% or more of clinical isolates are resistant to penicillin if a result of enzyme production. Rare isolates of enterococci also produce beta-lactamase. Gram-negative bacteria, including Enterobacteriaceae, P. aeruginosa, and Acinetobader spp. produce dozens of different beta-lactamase types that mediate resistance to one or more of the beta-lactam antibiotics.
Although the basic mechanism shown in Figure H-9 for beta-lactamase activity is the same for all types
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