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This chapter reviews the basic pharmacology of commonly prescribed antimicrobial agents used in the ED. Topics discussed are mechanisms of action, indications for use in the ED, contraindications, adverse drug reactions, dosage adjustments for renal or hepatic insufficiency, use in pregnancy, and important drug interactions. Additional information regarding the treatment of specific infections are found in other chapters of this text, and principles of drug interactions are discussed in Chapter e170.1, Principles of Drug Interactions.

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Effective antibacterial drugs have the ability to either inhibit the growth of (bacteriostatic effect) or kill (bactericidal effect) bacteria. Antibacterial effects result from a variety of mechanisms, including the inhibition of cell wall synthesis, inhibition of intrabacterial protein synthesis, alteration in nucleic acid metabolism, or intrabacterial enzyme inhibition (Table 158-1). A drug’s mechanism of action does not necessarily correlate with bacteriostatic or bactericidal effects, as these effects are also highly dependent on the concentration of antibiotic to which bacteria are exposed. Drugs of choice for most infections are not based on a bacteriostatic or bactericidal effect of an agent but rather on whether the drug reaches the site of infection in adequate quantities, the spectrum of the agent, its safety, and cost.

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Table 158-1 Mechanisms of Action of Antibacterial Drugs 
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Mechanisms of Action

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Cell Wall Active Agents

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β-lactam (penicillins, cephalosporins) and glycopeptide antibiotics (vancomycin, teicoplanin) must bind to receptors in the bacterial cell wall to cause an antibacterial effect. The target receptors (there are at least seven) for penicillins and cephalosporins are collectively called penicillin-binding proteins. Autolytic enzymes within the cell wall bind to penicillin-binding proteins, and the enzymes are activated, resulting in the deterioration of the peptidoglycan component of the cell wall, cell wall weakening, and eventual cell lysis. Glycopeptide antibiotics bind to a terminal dipeptide (alanine-alanine) in the cell wall peptidoglycan, and then, by steric hindrance, prevent the necessary cross-linking for a competent cell wall structure. At usual doses, β-lactam and glycopeptide antibiotics are bactericidal. Resistance can arise to these antibiotics due to mutations in the penicillin-binding proteins, leading to markedly reduced β-lactam binding (e.g., in oxacillin-resistant Staphylococcus aureus or penicillin-resistant Streptococcus pneumoniae), or when the terminal dipeptide mutates to a lactate-alanine (e.g., vancomycin-resistant Enterococcus faecium) that markedly reduces the level of vancomycin binding. Daptomycin inserts a lipophilic part of the molecule into the cell wall of gram-positive bacteria, depolarizing the cell wall, which causes the leakage of intracellular content, and a bactericidal effect.

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