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9: Antimicrobial Drugs

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    42520
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    Chapter 9 BSC 3271 Learning Outcomes

    • Tell the story of the discovery of antibiotics, including who discovered antibiotics, when, how, and the name of the first antibiotic discovered.
    • Define antibiotic and identify the specific group of microbes targeted by antibiotics.
    • Identify major targets of antibiotics and explain why disruption of each will cause microbial death or inactivation.
    • Describe desirable features of an antibiotic that would be used to treat infection.
    • Analyze a situation to identify the most suitable antibiotic/chemotherapy choice.
    • Explain the possible natural role of antibiotics in the environment and give an example of one bacterial genus that produces many clinically relevant antibiotics.
    • Describe the mode of action of beta-lactam antibiotics, including cellular structure impaired, what enzyme is inhibited and how that leads to impairment of cellular structure, consequences of impaired cellular structure, and whether growing cells are more easily killed or not and why.
    • Identify the cellular targets of the following antimicrobial drugs: beta-lactams, aminoglycosides, polymyxins, azoles, nucleotide analogs, and quinolones and which microbial groups they target (broad range, narrow range, which group(s) if narrow range) (which ones?).
    • Know to which class of antimicrobial drugs penicillins,  cephalosporins, carbapenems, streptomycin, colistin, fluconazole, acyclovir, and ciprofloxacin belong (beta-lactam, aminoglycoside, azole, polymyxin, or quinolone).
    • By its name, determine if an antibiotic is a penicillin, cephalosporin, or carbapenem.
    • By its name, determine whether an antibiotic is produced by Streptomyces
    • Explain the five common mechanisms of antibiotic resistance.
    • Describe the mechanism of beta-lactamase, including what kind of antibiotics this enzyme provides resistance to, how it provides resistance, and how the compound clavulanic acid counteracts beta-lactamase.
    • Explain why Pseudomonas species are naturally resistant to many different antibiotics.
    • Explain how natural selection leads to the emergence of antibiotic resistant strains of microbes.
    • List several human-controlled factors that contribute to the emergence of antibiotic resistance, including how antibiotics are used in health care and in agriculture.
    • Recognize the following abbreviations of antibiotic resistant pathogens and what the abbreviations stand for: MRSA, VRSA, VRE, CRE, MDR-TB, XDR-TB.
    • Describe strategies to reduce the spread of antibiotic resistance that can be used by 1. health care workers and 2. individuals.
    • Describe viral replication of HIV and how the replication mechanism can result in the development of drug resistance, particularly in the case of the nucleotide analog AZT.
    • Explain how the major anti-HIV drugs work and the advantages to  using combination drug therapy.

    • 9.1: Discovering Antimicrobial Drugs
      Antimicrobial drugs produced by purposeful fermentation and/or contained in plants have been used as traditional medicines in many cultures for millennia. The purposeful and systematic search for a chemical “magic bullet” that specifically target infectious microbes was initiated by Paul Ehrlich in the early 20th century. The discovery of the natural antibiotic, penicillin, by Alexander Fleming in 1928 started the modern age of antimicrobial discovery and research.
    • 9.2: Clinical Considerations
      Antimicrobial drugs can be bacteriostatic or bactericidal, and these characteristics are important considerations when selecting the most appropriate drug. The use of narrow-spectrum antimicrobial drugs is preferred in many cases to avoid superinfection and the development of antimicrobial resistance. Broad-spectrum antimicrobial use is warranted for serious systemic infections when there is no time to determine the causative agent or when narrow-spectrum antimicrobials fail.
    • 9.3: Antibiotics
      Antibacterial compounds exhibit selective toxicity, largely due to differences between prokaryotic and eukaryotic cell structure. Cell wall synthesis inhibitors, including the β-lactams, the glycopeptides, and bacitracin, interfere with peptidoglycan synthesis, making bacterial cells more prone to osmotic lysis. There are a variety of broad-spectrum, bacterial protein synthesis inhibitors that selectively target the prokaryotic 70S ribosome, including those that bind to the 30S and 50S subunits.
    • 9.4: Drugs Targeting Other Pathogens
      Because fungi, protozoans, and helminths are eukaryotic organisms like human cells, it is more challenging to develop antimicrobial drugs that specifically target them. Similarly, it is hard to target viruses because human viruses replicate inside of human cells.
    • 9.5: Antibiotic Resistance
      Antimicrobial resistance is on the rise and is the result of selection of drug-resistant strains in clinical environments, the overuse and misuse of antibacterials, the use of subtherapeutic doses of antibacterial drugs, and poor patient compliance with antibacterial drug therapies. Drug resistance genes are often carried on plasmids or in transposons that can undergo vertical transfer easily and between microbes through horizontal gene transfer.
    • 9.6: Testing Drug Effectivenes
      The Kirby-Bauer disk diffusion test helps determine the susceptibility of a microorganism to various antimicrobial drugs. However, the zones of inhibition measured must be correlated to known standards to determine susceptibility and resistance, and do not provide information on bactericidal versus bacteriostatic activity, or allow for direct comparison of drug potencies. Antibiograms are useful for monitoring local trends in antimicrobial resistance/susceptibility.

    Thumbnail: Staphylococcus aureus - Antibiotics Test plate. (Public Domain; CDC / Provider: Don Stalons).

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