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Antibiotics are soluble compounds produced by an organism that inhibit bacterial growth; the term also includes synthetic compounds such as fluoroquinolones. The majority of skin and soft-tissue infections (SSTI) are caused by Gram-positive organisms, most of which are susceptible to well-known agents with a relatively narrow spectrum of antimicrobial activity. In these cases, β-lactams, macrolides, and fluoroquinolones have been the mainstays of therapy.1 Increased use and misuse of these antibiotics has led to selection and propagation of resistant bacteria. Community-acquired resistant pathogens, such as methicillin-resistant Staphylococcus aureus (MRSA), have recently emerged as causes of SSTIs such as cellulitis, folliculitis, furunculosis, impetigo, erysipelas, and abscesses. More ominous is the emergence of complicated SSTIs with resistant pathogens, for example, MRSA and vancomycin-resistant Enterococci (VRE). Complicated cutaneous infections include those involving deeper tissues, those requiring surgical intervention, or those coincidental with underlying diseases that may complicate therapy. Combination therapy with well-established antimicrobials has been effective in many cases, and new antibiotics have broadened treatment options. However, given the relative paucity of new antimicrobials on the horizon, dermatologists are likely to be faced with growing treatment challenges. Understanding the pharmacologic properties of antibiotics ensures the most judicious use of these agents, and familiarity with antibiotic dosing schedules and adverse events will lead to therapeutic choices that achieve the highest degree of patient compliance.
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Antibiotics are largely classified by their chemical structures and subsequent mechanisms of action. Four major groups exist:
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Those that inhibit formation of bacterial cell walls, for example, the β-lactams (penicillins, cephalosporins, and carbapenems) and vancomycin; these are generally bacteriocidal.
Those that interfere with protein synthesis by binding to either the 50S or 30S bacterial ribosomal subunit may be bacteriostatic or bacteriocidal. Reversible binding (tetracyclines, macrolides, lincosamides, and linezolid) usually halts microbial growth, resulting in a bacteriostatic effect. Irreversible bacteriocidal binding occurs with aminoglycosides.
Those that interfere with bacterial nucleic acid synthesis, for example, rifampin (inhibits RNA polymerase), and quinolones (inhibit bacterial topoisomerase). These agents are typically bacteriocidal.
Those that interfere with key enzymes in folate metabolism, for example, trimethoprim and sulfonamides.
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Bacteriocidal versus Bacteriostatic Agents
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While antibiotics may be considered bactericidal (producing cell death) or bacteriostatic (halting cell growth or division), the distinction is ...