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