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inhibits bacterial cell walls non-toxic |
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drugs that use chemical against diseases |
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antimicrobial agents PRODUCED BY MICROBES that kill/inhibit the growth of other microbes |
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chem + bio - chems nudge microbes |
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Sulfanilomide 1st antimicrobial agent used to treat a variety of infections |
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magic bullets arsenic compound used to treat syphilis |
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penicillin inhibited staph |
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key to antimicrobial action |
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microbes w/ least amount of drugs for them |
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1. viruses- use host cell for life 2. eukaryotes (fungi + prot) bc they have similar cells to ours |
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Mode of action of antibiotics: Inhibition of cell wall synthesis |
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peter carried very purple bacteria in england: penicillins, cephalosporins, vancomycin, penems, bacitracin, isoniazid, ethambutol |
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Mode of action of antibiotics: inhibit protein synthesis |
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streptomycin, Erythromycin (macrolides), clindamycin, Kanamycin, Gentamicin, chloramphenicol, tetracyclines, aminoglycosides, |
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Mode of action of antibiotics: Inhibit Nucleic acid Metabolism |
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quinolones like ciprofloxacin (inhibit DNA gyrase), rifampin (inhibits DNA-directed RNA polymerase), sulfa drugs |
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Mode of action of antibiotics: Alter cell membrane permeability |
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Nystatin, Amphotericin B, Polymyxins (mostly anti-fungal, makes membranes leaky) |
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Mode of action of antibiotics: Inhibit Folic Acid Metabolism |
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Trimethroprim, Sulfonamides, these work because we can get Folic acid from food, they need to make it. |
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how does penicillin work? |
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it makes sloppy cross-bridges over NAG and NAM. Only works w/ actively growing cells |
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how do vancomycin and cycloserine work? |
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they interfere w/ particular alanine-alanine bridges that link NAM subunits in Gram-Positives |
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How does bacitracin work? |
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blocks secretion of NAG and NAM from cytoplasm- its in neosporin bc it works really well on group A strep, but is too toxic for anything but topical ointments |
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How do Isoniazid and ethambutol work? |
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they disrupt formation of arabinogalactan-mycolic acid in mycobacterial species (only hurts acid-fast cells like TB) |
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Which cells will inhibitors of cell wall synthesis not affect? |
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pant or animal (no peptidoglycan) |
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Why does the inhibition os Protein Synthesis work? |
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Prokaryotic ribosomes 70s Eukaryotic ribosomes 80s we can target prokaryotic ribosomes, the only problem is that the mitochondria in humans contains 70s ribosomes |
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how do aminoglycosides work? |
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change 3D shape of ribosomes -> mRNA is misread -> wrong amino acids used to make protein |
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how does Chloramphenicol work? |
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It bind to where the amino acids would have been added to the chain so no proteins are made |
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How does tetracycline work? |
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It blocks the docking site of the tRNA: no tRNA docking = no amino acid chain. |
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It binds to the ribosome and blocks the mRNA from moving through |
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How does amphotericin B (polyene) work? |
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It attaches to ergosterol found in fungal membranes and makes them leaky: affects fungi and sometimes cholesterol, but not bacteria (no sterols) |
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It disrupts the cytoplasmic membranes of Gram-negatives: it is toxic to human kidneys |
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How does Trimethoprim work? |
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It binds to enzyme involved in conversion of dihydrofolic acid to THF (we can eat folic acid, they NEED to make it, this stops them from making folic acid) |
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how do Amantadine, rimantadine, and weak organic bases work? |
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They target viral metabolism by neutralizing the acidity of phagolysosomes and preventing viral uncoating |
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ways to inhibit nucleic acid synthesis |
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block DNA replication or mRNA transcription interfere with function of nucleic acids (nucleotide analogs) viral DNA polymerases this method is effective against rapidly dividing cancer cells and viruses mostly because prokaryotic and eukaryotic DNA is pretty similar. |
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what does azidothymidine (AZT) treat and how? |
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first drug to treat HIV. cells can't replicate |
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To treat viruses, esp. In babies with RSV (a respiratory virus). |
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an example of a broad spectrum drug: |
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Diffusion Susceptability Test
isn't used anymore
Zone of inhibition |
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Minimum Inhibitory Concentration test
has turbid tubes and clear tubes.
->increasing concentration of drug ->
then get the organism away from the inhibitor to see if its dead or if it grows. |
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routes of administration and when to use |
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topical-external infection oral- simplest, health care provider doesn't need to administer, sometimes they don't take it, low concentration intramuscular-lower concentration than IV, need needle intravenous-need needle/catheter, drug concentration diminishes as liver and kidneys remove drug from blood |
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3 categories of side effects |
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toxicity, allergies, disruption of normal microbiota |
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Drugs like tetracycline can become toxic if expired. Drugs can be toxic to kidneys, liver, and nerves (like in middle ear) Need to be careful with pregnant women |
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rare, but can be life-threatening anaphylactic shock penicillin= common allergen |
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disruptions of normal microbiota |
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killed all the good guys can cause secondary infection, overgrowth of normal flora, big concern for hospitalized patients ex: yeast infections, black hairy tongue |
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2 ways to develop resistant bacteria |
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new mutations of chromosomal genes (natural selection)- other die, this one divides, makes a superbug microbes pass along drug resistance through R plasmids |
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2 ways bacteria alter drugs to make them ineffective |
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how to stop the creation of resistant strains: |
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higher concentrations of drug maintained in patient for long enough to kill all sensitive cells and inhibit others long enough for immune system to destroy. Be smart and finish antibiotic course. |
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