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Flashcards

Lecture 31 PMB

Candice Young Biology Inglês 36 flashcards

Flashcards do conjunto (36)

  1. 1Physical methods for microbial growth control--> temperature
    --> temperature and pressure
    --> UV/etc
    --> filters
  2. 2Chemical methods for microbial growth control--> disinfectants
    --> antiseptics
    --> antibiotics
  3. 3sterilizationREMOVAL of ALL living cells, spores, and viruses on an object
    the only method effective against bacterial endospores!
  4. 4disinfectionREMOVAL of PATHOGENS from INANIMATE surfaces
    chemical agents: 70% EtOH, bleach, strong ionic detergents
    do not put any of these in our body!!
  5. 5antiseptisREMOVAL of PATHOGENS from surface of LIVING TISSUE (ie. skin)
    chemical agents: 70% EtOH wipe, hydrogen peroxide, Neosporin, iodine containing compounds
  6. 6sanitationREDUCING microbial population to safe levels
  7. 7autoclaveused for heat/pressure sterilization
    --> steam achieves high T, rapidly kills everything
    --> takes about 20-40 minutes for required T to be reached by required time
  8. 8Pasteurizationprecisely controlled heat REDUCES microbial load, pathogen spread prevented
    --> reduced spoilage, longer shelf life
    --> does NOT kill all bacteria, just pathogens
  9. 9Flash Pasteurizationliquids flowing through heat exchanger raised to 71ºC for 15 sec --> rapid cooling
    --> milk has refrigerated shelf life of ~2 weeks after treatment
  10. 10Ultra-high temperature Pasteurization (UHT)liquid is heated to 135ºC for 1-2 sec (using continuous flow heat exchangers) --> also kills endospores --> products with an unrefrigerated shelf life of 6-9 months, if unopened
  11. 11What reduces the effectiveness of disinfectants/antiseptics?Organic material (dirt, biofilm, etc) can bind to/react with these to reduce their effectiveness
  12. 12Antimicrobial drugs/Antibioticschemicals used in humans that kill or inhibit the growth of microorganisms
    --> can be natural or synthetic
    --> must have SELECTIVE TOXICITY so the host is not harmed
  13. 13bacteriostatic growthgrowth is inhibited, but bacteria are NOT killed
    OD/direct visual count and viable cell count stay constant
    inhibitory molecules are at reversible binding equilibrium with a cellular protein, must keep agent at right concentration to constantly prevent growth!!
  14. 14bactericidal growthcells are killed, but not lysed
    OD/direct visual count constant, viable cell count decrease
    some irreversible damage to a protein or other component --> if agent is washed out/decreased, bacteria will still be dead
  15. 15bacteriolytic growthcells are killed and lysed
    OD/direct visual count decrease, viable cell count decrease
    usually do damage to the cell wall (PG) or cytoplasmic membrane --> if agent is washed out/decreased, bacteria will still be dead
  16. 16Minimal Inhibitory Concentration (MIC)lowest concentration of an agent that completely inhibits growth
    measured by a series of dilutions within culture medium, turbidity occurs in tubes with concentrations below the MIC
    compares the effects of different agents (as long as everything is standardized)
  17. 17Streptomyces antibiotic production--> production regulated by quorum sensing (G+ peptide system)
    --> occurs around time of sporulation, triggered by nutrient deprivation
    --> gives a competitive advantage against soil microbes
    --> resistant to own antibiotics
  18. 18spectrum of actiontells us which bacteria are affected
    narrow spectrum: very specific to harming only a certain species (ie. Isoniazid)
    broad spectrum : affects many types of microbes (Tetracycline, Sulfonamides, Cephalosporins, Quinolones)
  19. 19Mechanism of Action (MOA)tells us the specific molecular target that is
    bound/the process that is inhibited by the drug
    typical targets: cell wall, cytoplasmic membrane, DNA synthesis, RNA synthesis (tx), protein synthesis (tl), metabolism
  20. 20Examples of drugs that target well studied areasCell wall synthesis: penicillins
    Folic acid metabolism: sulfonamides
    Protein synthesis (30S): Tetracycline
    DNA gyrase: Cycloflaxin
  21. 21Target: cell wall biosynthesisMOA: B-lactam ring of Penicillin is suicide inhibitor of PBPs (perform transpeptidation in PG synthesis) --> BACTERIOLYTIC
    Spectrum: most effective agains G+ bacteria since they don't always cross OM
    -can have altered R groups: molecules more acid-stable, or β-lactamase resistant, or better at crossing OM of G- cells
  22. 22how B-lactam ring binds to PBPB-lactam ring is cysteine + valine, resembles D-ala-D-ala piece of PG --> PBP transpeptidase domain binds to this COVALENTLY, enzyme is inactivated
    peptide x-linking during PG synthesis
    blocked
  23. 23different steps of cell wall biosynthesis to be blockedD-Ala ligase - Cycloserine
    bactoprenol recycling - bacitracin
    transpeptidation - Penicillins,
    cephalosporins (D-Ala mimics) and Vancomycin (binds D-Ala-D-Ala)
  24. 24target: DNA supercoiling/replication/integrityMOA: Quinolones interact w/ bacterial DNA gyrase --> stabilize covalent intermediate between enzyme and DNA --> gyrase-DNA complex is roadblock for replication + creates broken ends --> irreversible damage to DNA, BACTERICIDAL
    Spectrum: both G+ and G-
    Ex: Ciprofloxacin, more soluble in fluorinated form
  25. 25DNA gyrasea topoisomerase II, makes ds breaks and introduces negative supercoiling
    found in ALL bacteria
    quinolone stabilizes covalent intermediate between DNA and gyrase --> blocks DNA replication
  26. 26target: MetabolismMOA: Growth factor analog, resembles PABA and blocks synthesis of folic acid; binds reversibly --> BACTERIOSTATIC
    Spectrum: G+ and G- bacteria
    Ex: Sulfanilamide
  27. 27folic acid and PABACells need folic acid as cofactor for single-carbon reduction rxns (used in nucleotide
    synthesis), and can't import it through bacterial cell membrane --> synthesize it from PABA, pteridine, and glutamic acid
    Sulfanilamide binds enzyme and attaches to pteridine, acts as a competitive inhibitor
  28. 28target: protein synthesisMOA: binds reversibly to 30S subunit of ribosome at A site --> prevents charged tRNA from entering --> BACTERIOSTATIC
    Spectrum: G+ and G-
    Ex: Tetracycline
  29. 29Napthacene ring system and protein synthesisBinds reversibly to 30S subunit of ribosome at the A site
    Tetracycline resembles this with two different R groups --> spectrum of activity (slightly diff drugs bind ribosomes
    of diff bacteria + diff drugs can taken up into cytoplasm of diffbacteria)
  30. 30all steps of protein synthesis and corresponding drugspremature peptide termination: Puromycin (mimics tRNA)
    peptide bond formation: Chloramphenicol
    (binds to 50s RNA)
    movement along mRNA: Erythromycin
    (binds to 50S rRNA)
    incoming tRNA: Tetracycline (binds to A site)
    mRNA reading accurately: Streptomycin (changes shape of 16S RNA)
  31. 31antibiotic resistance mechanisms1) Slightly alter the target so that the drug no longer binds
    (EX: point mutation in rpsL for protein S12)
    2) Modify the antibiotic so that it no longer binds the target
    (EX: nptI phosphorylates kanamycin, cat acetylates chloramphenicol, B-lactamases cleave B-lactam ring)
    3) Pump the drug out of the cell
    (EX: tatA catalyzes exchange of tetracycline out for protein in)
  32. 32Triclosanthought to be non-specific, disrupting membrane structure/function
    used in toothpaste, soaps, scrubs
    low water solubility but can be used in high concentrations in hydrophobic substances
  33. 33Triclosan resistance: experimental methodsperform genetic selections to identify mutant genes: make a genomic library from each resistant mutant --> select for plasmids that would confer increased resistance on WT strain
  34. 34results of Triclosan experimentsresistant mutants had pt. mutations --> a.a. subs in FabI (carrier protein reductase ENR involved in fatty acid (FA) biosynthesis that makes new cell membranes)
    MOA: Triclosan binds active site of FabI --> blocks FA biosynthesis --> arrests growth at LOW concentrations (0.1-20 μg/ml)
  35. 35Problems with Triclosan todayTriclosan is used at HIGH 2-20 mg/ml conc. in products and toothpaste + it’s a stable compound --> it’s accumulating in the environment + could disrupt the endocrine systems of fish and mammals + *some bacteria could become resistant by upregulating the expression of efflux pumps*
  36. 36Triclosan effect on efflux pumpsefflux pumps that have relaxed specificity could help bacteria pump out OTHER antimicrobials used to treat disease
    --> really bad

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Microbial Growth Control and Antibiotics
Criado por
Candice Young
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