BIOL 209 1st Edition Lecture22 Outline of Last Lecture I. Question/Answer’sII. DefinitionsIII. Disease ProgressIV. Killing Microorganisms V. Physical ControlVI. Chemical ControlVII. AntibioticsOutline of Current Lecture I. Question/Answer’sII. DefinitionsIII. Antimicrobial drugsIV. Antibiotic TargetsV. Sulfa DrugsVI. Antiviral DrugsVII. Antibiotic SensitivityVIII. Kirby Bauer TestCurrent LectureI. Question/Answer’sA. Do anti-cancer drugs have selective toxicity? No, they affect our normal cell division processes (chemotherapy)B. Inhibition of cell wall synthesis would selectively inhibit microbial growth- Cell wall synthesis is unique to microbial cells (compared to eukaryotic cells)C. Why don’t sulfa drugs block biosynthetic pathways in OUR cells? We get folic acid from our diet – we don’t use this pathway, so blocking of these steps won’t affect usD. Mutation of which would be least likely to resist antibiotics? A member of the ETSE. Why do different microbes show different sensitivities to the same antibiotic? Gram +/- = differences in structures, so differences in susceptibilitiesII. DefinitionsA. Selective toxicity: a primary factor determining usefulness of antibiotics is their ability to target structures and processes that are specific to microorganismsIII. Antimicrobial drugsA. TargetsThese notes represent a detailed interpretation of the professor’s lecture. GradeBuddy is best used as a supplement to your own notes, not as a substitute.1. Cell wall, cell membrane, nucleic acid & protein synthesis, and some metabolic pathwaysIII. PenicillinA. Synthesis of peptidoglycan cell walls is targeted by Penicillin and Cephalosporin derivatives, which block glycan chain cross-links1. Glycan chains are composed of alternating N-acetyl glucosamine and N-acetyl muramic acida. A short peptide bridge links the glycan chainsB. Derivatives1. Core beta-lactam ring is modified with a variety of chemical groups that alter drug characteristics without changing its target of actiona. Many new drugs are generated this wayIV. Antibiotic TargetsA. Antibiotics can bind to specific phospholipids or sterols to disrupt microbial membranes1. Polymyxins target bacterial membranes2. Polyenes target fungal membranesB. Antibiotics can target nucleic acid synthesis1. Ciprofloxacin inhibits bacterial helicases necessary for DNA synthesis, and rifamin inhibits RNA polymerase activity blocking transcription2. They can target ribosome function including mRNA decoding, tRNA binding, peptide bond formation, and ribosome translocation during protein synthesisa. Know examples from textV. Sulfa DrugsA. Act as competitive inhibitors of an enzyme required for the synthesis of folic acid (a coenzyme essential for biosynthetic pathways)VI. Antiviral DrugsA. Tamiflu blocks influenza virus entry and release from the cell B. Nucleoside analogs (AZT) and enzyme inhibitors block function of reverse transcriptase polymerase preventing HIV genome replication1. HIV protease inhibitors block production of new viral particles by blocking processing of viral polyproteinVII. Antibiotic SensitivityA. Varies substantially between species, and between strains with the same species1. Minimal inhibitory concentration (MIC) is the lowest concentration required for complete inhibition of growthVIII. Kirby Bauer TestA. Used to measure sensitivity to a series of antibiotics – the extent of growth inhibition indicates the degree of sensitivity1. In some cases, enhanced killing by exposure to two antibiotics may be observed as an extended zone of inhibition between adjacent antibiotic carrier discsB. Natural resistance1. No target2. No accessC. Acquired resistance1. Inactivation of antibiotic2. Removal of antibiotic3. Reduced access of antibiotic4. Modification of target of antibiotic5. Develop alternate