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Auburn University
BIOL 3200

ANTIBIOTICS • o Antibiotic resistance o How do they work o How do we produce them o Are they overprescribed o Why might they make you sick o How are they mass produced o How were they discovered o How do we continue to discover them • Prokaryotic diversity has allowed organisms to survive in multiple niches. What are the choices when others invade your space? o Eat something else o Find a new home o Kill everyone • History of antimicrobial drugs o Arsenic compounds early examples of man-made “selective” antimicrobial o Alexander Fleming- noticed “microbes killing microbes” later termed antibiotics  Discovered penicillin while working with Staphylococcus, identified mold as penicillin o Chain and florey purified active penicillin o Selman Waksman isolated streptomycin from soil bacterium Streptomyces griseous • Features of antimicrobial drugs o Antimicrobial action  Drugs may kill or inhibit bacteria growth • Inhibit growth- bacteriostatic • Kill- bactericidal  Bacteriostatic drugs rely on host immunity to eliminate pathogen  Bacteriocidal drugs are useful in situations when host defenses cannot be relied upon to control pathogen o Most modern antibiotics come from organisms living in the soil  Isolates from bacterial species Streptomyces and Bacillus as well as fungi Penicillium and Cephalosporium  Many and good, BUT of course man-made derivatives have been added to the repertoire o Selective toxicity  Antibiotics cause greater harm to microorganisms that to human host • Generally by interfering with biological structures of biochemical processes common to bacteria but not humans • Spectrum of activity o Antimicrobials vary with respect to range of organisms controlled  Narrow spectrum • G + OR G- only  Broad spectrum • G+ AND G-  Disadvantage of broad spectrum is disruption of normal flora o Antimicrobial resistance  Microorganisms have innate of adaptive resistance to antibiotics • Mechanisms of action o Inhibition of cell wall synthesis o Inhibition of protein synthesis o Inhibition of nucleic acid synthesis o Inhibition of metabolic pathways o Interference with cell membrane integrity o Interference with essential processes of M. tuberculosis • Inhibition of cell wall synthesis o Peptidoglycan cell wall unique to bacteria o Antimicrobials of this class:  B-lactam drugs- the penicillin’s  Vancomycin  Bacitracin • Mechanisms of action o The penicillins  Each member has common structure • Modified side chains create derivatives  Penicillin drugs used to include • Natural penicillins • Broad-spectrum penicillins • Extended spectrum • Penicillinase-resistant • Combination therapy penicillins + β lactamase inhibitor • Penicillins and caphalosporins o These drugs called β –lactams o Inhibit peptide bridge formation between molecules of ptg  Competitively inhibits function of penicillin-binding proteins o Some org. resist effects through production of b-lactamase enzyme o Others LOOK AT SLIDE FOR MISSED CLASS 1. Antibiotic resistance 2. How do they work 3. What produces them 4. Over-prescription 5. Allergies? 6. Affect on microflora 7. Mass production • Inhibition of protein synthesis o Proteins are synthesized on ribosome • Differences in prokaryotic (70s) and eukaryotic (80s) ribosomes are responsible for selec ve toxicity  Drugs of this class include • Aminoglycosides • Tetracyclines • Macrolides • Chloramphenicol • Lincosamides • Oxazolidinones • Streptogramins o Prokaryotic kill prokaryotes “are we so different?”  What are the possible targets and considerations • Peptidoglycan • Ribosome o Inside cell • Tetracyclines o Reversibly bind 30S ribosomal subunit  Blocks attachment of tRNA to ribosome • Prevents continuation of protein synthesis o Effective against certain gram + and gram – o Newer tetracyclines such as doxycycline (deriv
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