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Antibiotics
Microbiology I - Exam 2 - Antibiotics
| Question | Answer |
|---|---|
| What is the theraputic ratio formula? | toxic dose/therapeutic dose - aka, concentration toxic to host/concentration toxic to pathogen |
| What is better: a high or low theraputic ratio? | high |
| Type of antiobiotic that kills | bacteriocidal |
| Type of antiobiotic that stops growth | bacteriostatic |
| MBC stands for | minimum bacteriocidal concentration |
| MIC stands for | minimal inhibitory concentration |
| Lowest concentration that inhibits visibal growth on plates (lawns) or in liquid culture (turbidity). | mic |
| Lowest concentration that kills 99.9% of bacteria in a given time | mbc |
| What percent of bacteria must be killed to satisfy MBC? | 99.9 |
| An example of an antibiotic with a high therapeutic ratio: | penecillin |
| An example of an antibiotic with a low therapeutic ratio: | azt |
| What is a good way to ensure a high therapeutic ratio? | target mechanisms that host does not posses |
| An example of an antibiotic with a ZERO therapeutic ratio: | ethanol or H2O2 or bleach |
| What test is used to determine MIC? | kirby bauer |
| Can Kirby-Bauer test definitively indicate the Minimal Inhibitory Concentration? | no, other factors include: bacterial growth rate, diffusion rate of antibiotic, conditions of growth |
| Can Kirby-Bauer test tell which of several antibiotics is most effective? | no, diffusion rates in medium may be different |
| An example of a biological factor that can have a positive effect on the concentration of antibiotics in mammals: | concentration of drug in urinary tract - makes treating UTI or kidney infection easier - need less drug |
| An example of a biological factor that can have a negative effect on the concentration of antibiotics in mammals: | difficulty crossing blood-brain barrier |
| Endocardium, brain, and spine are not easily accessed by the immune system. What type of antibiotic must be used? | bacteriocidal |
| Three main mechanisms of resistance: | change target, limit access to target, destroy antibiotic (mutation, permeability, enzymes) |
| What is one mechanism that bacteria use to limit access of antiobiotics to target? | efflux pumps |
| How do efflux pumps work? | bind to antibiotic and eject from cytoplasm |
| Three enzymes that destroy (or modify) antibiotics: | beta lactamase, CAT, AME |
| Another name for penecillins | beta lactams |
| Another name for beta lactams | penecillins |
| Who discovered penecillin? What year? | fleming, 1928 |
| Penecillins are structural analogs of ______. | d-amino acids (d-alanine, d-alanyl) |
| What enzyme makes cross-links in peptidoglycan layers of cell wall? | transpeptidase |
| What amino acid is incorporated in the cross-links between peptidoglycan layers of the cell wall? | d-alanine |
| What is the target for penicillins? What do they inhibit? | transpeptidase, cell wall formation |
| What enzymes destroy penecillins? | beta lactamases |
| What is a resistance mechanism against penecillins? | beta lactamase enzymes |
| Where are beta lactamases found in Gm (-) bacteria? | periplasmic space |
| Where are beta lactamases found in Gm (+) bacteria? | secreted into medium |
| What type of bacteria is able to more effectively use beta lactamases? Gm (-) or Gm (+)? | Gm (-) [Gm (+) secrete beta lactamase into medium where it diffuses away] |
| How does beta lactamase destroy penecillin? | opens the 4-membered ring |
| How many classes of beta lactamase are there? | 4, with different properties, specificities |
| What is the name of the drug that combines a beta lactam with a beta lactamase inhibitor? | augmentin |
| What are the ingredients of Augmentin? | amoxicillin, clavulonate (beta lactam + beta lactamase inhibitor) |
| What is the target of clavulonate? What does is inhibit? | beta lactamase, destruction of another beta lactam (binds to it before it can destroy amoxicillin) |
| What type of compound is clavulonate? | beta lactam - you could call it a 'structural analog' |
| The newer subclass of beta lactams that have the same target | cephalosporins (not technically beta lactams, but similar) |
| What are two advantages of cephalosoprins over beta lactams? | improved activity against gm-, resistance to beta lactamase |
| What is one of the most widely used types of antibiotics? | cephalosporins |
| Folates are necessary to synthesize what biological molecule? | thymidine (tetrahydrofolate catalyzes carbon transfer to convert dUMP -> dTTP) |
| Without folates, what ultimately cannot be produced? | dna |
| Sulfa drugs (sulfonamides) are structural analogs of ____. | paba (para-aminobenzoic acid) |
| What is PABA? | para-aminobenzoic acid |
| Beta lactams are structural analogs of _____. | d-alanine |
| First generation cephalosporins are more effective against Gm (__) bacteria. | + |
| What is the important pathway that starts with PABA? | PABA -> DHF -> THF -> thymidine -> DNA |
| What two drugs inhibit folate production? | sulfa drugs, trimethoprim (they work together synergistically) |
| What enzyme converts DHF to THF? | dihydrofolate reductase (DHFR) |
| What are three reasons to use combination therapy (two or more antibiotics)? | prevent resistance, emergencies, synergy |
| What is a reason to avoid combination therapy (two or more antibiotics)? | negative interactions |
| What two drugs should not be mixed? | chloramphenicols, aminoglycosides |
| What kind of drug is inhibited by bacteriostatic antibiotics? | drugs that require growth to work (usually bacteriocidal) |
| The chance of developing spontaneous resistance is | 1/10 e+6 |
| With combination therapy, what is the chance of developing spontaneous resistance? | 1/10 e+12 (chance of developing spontaneous resistance is SQUARED!) |
| Name two drugs that work synergystically on the same pathway. | sulfa drugs, trimethoprim |
| Name two drugs that work synergystically on different pathways with penecillin. | chloramphenicols, aminoglycosides |
| What is the target for chloramphenicols? What do they inhibit? | 50s ribosomal subunit, peptide synthesis |
| Are chloramphenicols bacteriostatic or bacteriocidal? | bacteriostatic MOSTLY, but could be bacteriocidal |
| What other drug is often combined with chloramphenicol? | penecillin |
| Do chloramphenicols have a good therapeutic ratio? Why? | no, toxic to bone marrow |
| Do sulfa drugs have a good therapeutic ratio? Why? | yes, humans can absorb folates through cell membrane via active transport |
| Do beta lactams have a good therapeutic ratio? Why? | yes, humans have no cell wall |
| Why are chloramphenicols only rarely used? | chance of developing fatal aplastic anemia - probably due to inhibition of mitochondrial protein synthesis - mitochondria are similar to bacteria |
| What are two resistance mechanisms against chloramphenicol? | chloramphenicol acetyl transferase (CAT), ribosomal mutation |
| What is a resistance mechanism against trimethoprim? | mutation of DHFR or alternate DHFR |
| What is the target of cephalsporins? | transpeptidase (similar to beta lactams) |
| What is the target of tetracyclines? What do they inhibit? | 30s ribosomal subunit, binding of trna (codon:anticodon) |
| Do tetracyclines have a good therapeutic ratio? Why? | yes, drug affects host, but bacterial active transport system increases concentrations greatly |
| What is a resistance mechanism to tetracycline? | mutation of bacterial active transport system (drug still works, but concentrations are too low to have much effect) |
| What is an example of a macrolide? | erythromycin, lincomycin |
| What is the target of macrolides? What do they inhibit? | 50s ribosomal subunit, progression of nascent polypeptide - jams right in the middle, sterically blocks new peptide |
| What is a resistance mechanism against macrolides? | mutation of ribosome so that binding no longer occurs |
| What is the target of rifamycin? What does it inhibit? | rna polymerase, transcription |
| What does RNA polymerase use to bind to a nucleotide? | Mg++ binds to two phosphates |
| How does rifamycin inhibit transcription? | displaces Mg++, prevents rna pol from binding to phosphates on nucleotide |
| What disease is rifamycin used against? | Tb, other mycobacterial diseases (Broad Spectrum!) |
| What is a resistance mechanism against rifamycin? | mutation of rna pol |
| What drugs target cell wall synthesis? | beta lactams, cephalosporins |
| What drugs target protein synthesis? | chloramphenicols (50s), macrolides (50s), tetracylines (30s) |
| What drugs target DNA replication | quinolones |
| What is the target of quinolines? What do they inhbit? | DNA gyrase, relaxation of supercoiling |
| What drugs target nucleic acid synthesis? | sulfa drugs, trimethoprim |
| What drugs target RNA synthesis? | rifamycin, rifampin |
| What drugs target membranes? | polymixins, detergents, ionophores |
| What is the target of polymixins? | cell membranes |
| Do polymixins have a good therapeutic ratio? Why? | no, neurotoxic, nephrotoxic - use only in extreme circumstances or topically |
| How do polymixins work? | make cell membranes leaky (large cyclic protein head, long hydrophobic tail) |
| What is the target of detergents? | cell membrane |
| Do detergents have a good therapeutic ratio? Why? | no, membranes are same in humans and bacteria - use only on skin, cells are already dead |
| Disinfectant/Antiseptic: how does alcohol work? | denatures proteins at 70% concentration |
| Disinfectant/Antiseptic: how does silver, colloidal silver work? | binds proteins in cell membranes, interferes with respiration (takes place at membranes) |
| What is silver nitrate used to treat? | eye infections |
| What is colloidal silver used to treat? | bed sores |
| Disinfectant/Antiseptic: how does Triclosan work? | inhibits fatty acid biosynthesis - very good specificity - could be antibiotic in the future |
| Where is triclosan found? | soaps, toothpastes, mouthwash, shampoo |
| Disinfectant/Antiseptic: How does iodine work? | binds to histidine, tyrosine, tryptophan (all have ring structures), denatures proteins, highly effective against viruses, fungi, spores |
| Disinfectant/Antiseptic: will 70% alcohol kills spores? | no |
| Disinfectant/Antiseptic: what will work on spores? | iodine |
| Disinfectant/Antiseptic: How does hydrogen peroxide work? | releases oxygen, creates radicals, effervesces, effervescence lifts away fomites |
| Disinfectant/Antiseptic: How does benzalkonium chloride work? | probably denatures proteins, destabilizes membranes |
| Disinfectant/Antiseptic: What is benzalkonium chloride? | quaternary ammonium (NR4), surfactant, hand scrub, facial wash |
| Disinfectant/Antiseptic: How does formaldehyde work? | very reactive with proteins and nucliec acids, cross-links P-P and N-N with covalent bonds, can wipe out a genome! |
| Disinfectant/Antiseptic: How is formaldehyde used? | preservative, fixative for tissues (but not for tissues whose genetic material needs to be preserved) |
| Disinfectant/Antiseptic: How does irradiation work? | causes double strand breaks to DNA (only takes 2 breaks to kill) |
| Resistance: intrinsic resistance is due to | specificity of antibiotic, self-made antibiotics |
| Disinfectant/Antiseptic: how does alcohol work? | denatures protein at 70% concentration |
| Resistance: genes for resistance are found | both chromosome and plasmids |
| Resistance: resistance genes on the main chromosome typically code for | structural changes (e.g., changes to antiobiotic targets) |
| Resistance: resistance genes on plasmids typically code for | resistance enzymes (e.g., destroy antibiotic) |
| Resistance: are resistance genes on the main chromosome mobile? | not usually, but they can be transferred |
| Resistance: what are some ways that microbes are being exposed to drugs in the environment? | antibiotics given without need (60% of sore throats are viral), use of braod spectrum antibiotics instead of narrow, improper dosage, agriculture, population size and density, aerosolized antibiotics from needles |
| Resistance: why are broad spectrum antibiotics over-used? | to save cost and time in identifying specific bacteria |
| Resistance: what is the problem with overuse of broad spectrum antibiotics? | exposes all normal flora to the drug and forces them to develop resistance (once bacterial resistance is developed by ANY bacteria, it can spread to other species) |
| Resistance: what are two sources of improper dosage of antibiotics? | OTC antibiotics, patient compliance |
| Resistance: what are the two modes of acquisition of resistance genes? | vertical (inherited) and horizontal (transmitted) |
| Resistance: what is a transposon | mobile DNA element that codes for its own integrase enzyme and can integrate into a chromosome |
| Resistance: what is Tn21 | a single transposon that is resistant to 5 drugs |
| Resistance: what are 'R factors'? | resistance-encoding plasmids |
| Resistance: what are plasmids | autonomouly replicating, extrachromosomal circular DNA |
| Resistance: can plasmids move between species? | YES |
| Resistance: what is an MDR plasmid? | multi-drug resistant |
| Resistance: what is pRSB101 | an MDR plasmid (5 genes for resistance!) found in sewage |
| Resistance: which is the lethal strain of E. coli? | O157:H7 |
| Resistance: what percent of E. coli O157:H7 is resistant to two or more antibiotics? | up to 45% |
| Resistance: characterize antibiotic use in high population density | fast spread of disease (aerosols), high need of antibiotics to curb spread, fast emergence of resistance (including among normal flora), fast spread of resistance |
| Resistance: what microbe is considered the KING of resistance | Staphylococcus aureus, present on the skin of ~10% of population, can infect any part of body |
| Resistance: what is the top cause of hospital infections? | Staph aureus |
| Resistance: what is MRSA? | methycillin resistant Staph aureus |
| Resistance: what is VRSA? | vancomycin resistan Staph aureus |
| Resistance: what are two strategies to curb the development of resistance? | limit environmental exposure, withhold new drugs |
| Resistance: what is D.O.T.? | Directly Observed Therapy - a way to ensure patient compliance with a course of antibiotics |
| Resistance: why is is difficult to withold new drugs? | pharmaceutical companies are not inclined to develop a new drug if they can't sell lots of it |
| Resistance: what is the current "last resort" drug? | zyvox |
| Drug Design: What is "Rational Drug Design"? | identifying specific processes and structures and developing drugs for those specific targets |
| Drug Design: how can the configuration of the target be determined? | X-ray crystallography. Allows the precise determination of the shape of a (crystallized) protein. Can determine exactly where a drug should go and how it should be shaped to fit. |
| Drug Design: how can the ideal inhibiting molecule be identified? | computer modeling and computer database of known molecules |
| Drug Design: what makes a better drug, a large or small molecule? | small molecules: will diffuse better, cross blood-brain barrier, cross cellular membranes |
| How do beta lactams differ? | different side chains, same nucleus |
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epiphenom
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