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MSU MMG 301 - Lecture 33

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Lecture 331. Be able to describe toxic dose and therapeutic dosea. Toxic dose- Level at which a drug becomes toxic to the hostb. Therapeutic dose- Required for effective clinical treatment2. Understand broad vs. narrow spectrum antibioticsa. Narrow- Ones that work on more specific organisms (isoniazid, poymyxins)b. Broad- Work on greater variety of organisms (tetracycline)c.3. Know what critical pathways in bacteria are inhibited by the antibiotics discussed in class a. Inhibition of a critical biochemical metabolic pathwayb. Inhibition of DNA/RNA synthesisi. Quinolones- inhibitors of DNA gyrase (required for supercoiling of DNA) 1. Block bacterial cell division c. Inhibition of cell wall synthesisi. Cephalosporinsd. Inhibition of translationi. aminoglycoside- binds to 30S subunit of bacterial ribosomes (ex. kanamycin)ii. macrolide- bind to 50S subunit of bacterial ribosomes (ex. erythromycin)iii. tetracyclines- bind to 30S subunit of bacterial ribosomese. Alteration of cell membranes i. daptomycin- aggregates and inserts into cytoplasmic membrane, proton motive force is lost and cell diesii. plastensimycin- inhibits an enzyme critical for fatty acid synthesis1. cells can’t synthesize lipids and eventually die4. Know how sulfanilamide, isoniazid, and quinolones are growth factoranalogs and what pathways they inhibit a. Sulfanilamide- Blocks nucleic acid synthesis by blocking enzyme, inhibits pathway for nucleic acid synthesisi. Growth factor analog of p-aminobenzoic acidb. Isoniazid- block synthesis of mycolic acids, used for TB treatmenti. Growth factor analog of nicotinamideii. Inhibits pathway for synthesis of mycolic acidsc. Quinolones- inhibitors of DNA gyrase (required for supercoiling of DNA) i. Block bacterial cell division 5. Be able to describe what bacterial enzyme is inhibited by β- lactam antibiotics and be able to identify a generalized chemical structure of a β-lactam antibiotic a. Inhibits transpeptidase b.6. Know the three classes of antibiotics that bind to bacterial ribosomes, and the example of each class a. Aminoglycoside antibiotics such as Kanamycin bind to bacterial ribosomesb. Macrolide antibiotics such as erythromycin bind to bacterial ribosomesc. Tetracyclines also bind to ribosomesi. Many semisynthetic derivatives (different R groups) have been found7. Understand how an ionophore antibiotic such as daptomycin works to kill bacteriaa. an ionophore antibioticb. cyclic lipopeptide that aggregates and inserts into the cytoplasmic membranec. creates pores in the membrane that result in a de-energized membraned. proton-motive force is lost and cell dies due to lack of energy 8. Know the mechanisms of resistance presented in lecture a. 1. Reduced permeability of the antibiotic (penicillin G)b. 2. Inactivation of the antibiotic by a bacterial enzyme (beta-lactam antibiotics)c. 3. Mutation in the antibiotic target (erythromycin)d. 4. Development of a metabolic bypass in a pathwaye. 5. Efflux pump- membrane pump that makes sure antibiotic concentration in the cell stays low (tetracycline)9. Review the examples of antibiotic resistant bacterial threatsa. Methicillin-resistant Staphylococcus aureus (MRSA)i. Originally named because of resistance to a semi-synthetic penicillin.ii. A skin pathogen that can become invasive.iii. Some clinical isolates are resistant to almost all antibiotics.iv. A problem in healthcare settings.b. Vancomycin-resistant Enterococcus (VRE)i. Enterococcus inhabits human intestinal and female genital tract, but can also cause infections at other sites.ii. Are resistant to vancomycin and other antibiotics.iii. Most VREs occur in hospitals.iv. Usually occur in patientsc. Many others:i. Multi-drug resistant Mycobacterium tuberculosis (MDR-TB)ii. Carbapenem-resistant Enterobacteriaceae (CRE)iii. Clostridium difficile: not an antibiotic resistance problem, but infections occur in patients treated with antibiotics.10. Define selective pressure in the context of antibiotic resistancea. From using antibiotics so much and so frequently over the years we’ve created an enhanced population of bacteria that are resistant 11. Know what can be done to reduce the increase of antibiotic resistant bacteria in clinical settings a. Reduction in the use of antibioticsb. Increased development of new


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MSU MMG 301 - Lecture 33

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