Abstract
Anti-bacterial drugs work by exploiting differences between mammalian and microbial physiologic processes. Since bacteria, unlike mammals, have cell walls, many anti-bacterial agents work by binding to components of the cell wall or inhibiting the synthesis of the cell wall. These agents include the beta-lactam and glycopeptide antibiotics. Other anti-bacterial agents function by exploiting differences in DNA replication (the quinolones inhibit DNA gyrases that are used in bacterial replication) or transcription (rifampicin). Still other agents exploit differences in the translational process, as bacteria use ribosomes that are different from mammalian ribosomes. The macrolides, tetracyclines, and aminoglycoside antibiotics exert their anti-bacterial effects by binding to different components of the bacterial ribosome (see Fig. 2.1). Still other anti-microbial agents such as the sulfonamides function by exploiting differences in the metabolic pathways between mammals and bacteria. Since bacteria are unable to use folic acid but must synthesize it from para-aminobenzoic acid, drugs that inhibit this pathway will selectively inhibit bacterial growth without toxicity to mammalian cells.
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Finberg, R.W., Guharoy, R. (2012). Basic Principles of Drug Delivery and Dosing. In: Clinical Use of Anti-infective Agents. Springer, New York, NY. https://doi.org/10.1007/978-1-4614-1068-3_2
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DOI: https://doi.org/10.1007/978-1-4614-1068-3_2
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