Microbiology Ch 20

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cswett
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80084
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Microbiology Ch 20
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2011-04-17 21:48:35
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Micro Antimicrobial Drugs
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Worksheet questions for Micro Ch 20 on Drugs
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  1. Secective toxicity
    drug that kills pathogen withough damaging the host
  2. Antibiotic
    • substance made by a microbe that inhibits growth of another microbe
    • (sulfa drugs are not technically antibiotics but are usually included)
  3. chemotherapy
    the use of drugs to treat a disease
  4. Penicillin
    • Discovered in 1928
    • Used clinically in 1940 for the 1st time
  5. 3 sources of antibiotics
    1. bacteria - 50% of all antibiotis are from streptomyres

    2. fugus - penicillin, cephalosporins

    3. synthetic - sulfa drugs
  6. 1. Why are gram (-) bacteria harder to kill than gram (+)?
    2. Are mycobacteria hard to kill?
    3. Are fungi hard to kill?
    4. Are viruses hard to kill?
    1. Gram(-) have outer membrane with porins that only let small molecules in

    2. Mycobacteria have mycolic acid in their cell wall - drugs cant penetrate it

    3. Fungi are a eukaryotic pathogen - same cell type as host - may damage host

    4. Viruses live inside host cell - hard to kill w/o damaging host
  7. Broad spectrum antibiotics
    affects a wide range of microbes - Gram (+) & Gram (-)
  8. Superinfection
    results from antibiotic killing off normal flora - bacterial overgrowth of a pathogen
  9. bacteriocidal
    bacteriostatic
    bactericidal - antibiotic that KILLS bacteria - requires bacterial growth to work

    bacteriostatic - antibiotic that prevents (or limits) bacterial growth - allows hosts immune system to work - requires that the host's immune system is competent
  10. 5 ways that antibiotics work
    1. inhibit cell wall synthesis - bacteria - penicillin blocks peptidoglycan cross links - cell lysis

    2. inhibit protein synthesis -bacteria -block normal function of 70S ribosome - could cause problem because mitochondria bacuse they ahve 70 S ribosomes

    3. Injure cell membrane - bacteria/ fungus - alter selective permeability (binds to sterols on fungus)

    4. Inhibit DNA/ RNA synthesis - blocks DNA replication or RNA transcription

    5. Inhibit synthesis of essential metabolites - blocks folic acid synthsis - can't make nitrogenous bases
  11. What is the difference between prokaryotic and eukaryotic ribosomes?
    • Prokaryotic cells = 70S ribosomes
    • 50 + 30 = 70 S (Svedberg)

    Eukaryotic cells = 80S ribosomes

    Svedberg unit is based on rate of sedimentation in a high-speed centerfuge
  12. List 5 ways antibiotics work and give examples of drugs
    • 1. Cell wall disruption
    • - peninillin
    • - cephalosporins
    • - bacitracin
    • - vancomycin
    • - anti TB drugs - INH and Ethambutol (block mycolic acid synthesis)

    • 2. Protein synthesis disruption
    • - chloramphenicol
    • - aminoglycosides
    • - tetracyclines
    • - macrolides (erythromycin)

    • 3. Cell membrane disruption
    • - polymyxin
    • - antifungals : amphotericin, ketoconozole

    • 4. DNA/ RNA synthesis disruption
    • - rifampin - DNA replication
    • - quinolones (cipro) - RNA transcription

    • 5. Vital Metabolite synthesis disruption
    • - sulfonamides (sulfa) - bactrim
  13. Characteristics of Penicillins (Pcn)
    • CELL WALL DISRUPTION
    • Penicillin - has a "nucleus" = all penicillins have a Beta lactam ring structure with different R goups attached

    Works by preventing peptidoglycan cross bridges from forming - most work best on Gram (+)

    • Penicillinase - enzyme made my some bacteria that inactivate PCN by cleaving the Beta lactam ring
  14. Penicillins -PCN or pen
    • CELL WALL DISRUPTION
    • Work by messing with peptidoglycan

    • Natural penicillins:
    • a. Pen G = IV (narrow)
    • b. Pen V = (PO) - stable in stomach acid
    • c. procaine Pcn - lasts longer - given deep IM in a suspension w/ local anesthetic

    • Semisynthetic penicillins:
    • narrow spectrum - Gram (+)
    • 1. methicillin - penicillinase resistant penicillin - can cause MRSA (no longer used much)
    • MRSA = methacillin resistant staph aureus
    • 2. oxacillin - penicillinase resistant pcn

    • Broad spectrum - polar group added so it can penetrate outer membrane on Gram (-)
    • 1. ampicillin
    • 2. amoxicillin
    • 3. ticarcillin

    Augmentin - amoxicillin + penicillinase inhibitor

    Primaxin - last generation - very powerful - kills 98% of hospital microbes

    Monobactam - newer selective killer - pseudomonas, E. coli
  15. Cephalosporins
    • CELL WALL DISRUPTION
    • -Penicillin- like structure - beta lactam ring- all are penecillinase resistant
    • - kill by messing with peptidoglycan
    • - made from a fungu
    • - many are semi-synthetic
    • - each generation is more effective against Gram (-) and has a broader spectrum of activity

    • 1st generation:
    • 1. Ancef (IV)- cetazolin
    • 2. Keflex - po - cetatexin

    • 2nd gen:
    • 3. Cettin - cefuroxime
    • 4. Zinacef

    • 3rd gen:
    • 5. Rocephin
    • 6. Claforan

    • 4th gen - broadest spectrum
    • 7. Maxipime
  16. Polypeptide antibiotics (small proteins)
    • CELL WALL DISRUPTION
    • 1. Bacitracin - bacillus from Tracy's wound
    • - narrow spectrum -Gram (+) topical ointment
    • - Block pepdidoglycan synthesis

    • 2. Vancomycin - to vanquish
    • - very narrow but KILLS MRSA
    • - but VRE not exists - no Rx for some VRE
    • - - VRE = Vancomycin Resistant Enterocicci
  17. Antimycobacterial antibiotics
    • CELL WALL DISRUPTION
    • inhibit mycolic acid in cell wall

    • 1. Isoniazid (INH) - Rx for M. tuberculosis
    • - 1st line treatment for TB - 1 year Tx
    • - Can cause drug hepatitis
    • - effect mycobacteria only
    • - penetrates macrophages & walled off tissue

    • 2. Ethambutol - Rx for TB
    • - inhibits incorporation of mycolic acid in cell wall
    • - 2nd line drug for TB
    • - effects mycobacteria only
  18. Chloramphenicol (CAM)
    • INHIBITS PROTEIN SYNTHESIS
    • 70S ribosome inhibitors (50S + 30S)
    • Broad Spectrum -

    • *bacteriostatic - binds to 50S & stops peptide bond formation
    • - inexpensive
    • - toxic - can cause aplactic anemia (no blood cell production - rare)
  19. Aminoglycosides
    • INHIBITS PROTEIN SYNTHESIS
    • - best for Gram (-)
    • - - bind to 30S & stop peptide bond formation
    • - - Toxic - ototoxic (auditory nerve) & nephrotoxic (renal failure) - must monitor blood levels

    • Streptomycin
    • Neomycin
    • Gentamycin (IV)
    • Tobramycin (IV)
  20. Tetracyclines
    • INHIBITS PROTEIN SYNTHESIS
    • *Broad spectrum - bacteriostatic
    • *Interferes with tRNA attachment to mRNA on ribosome 30S
    • *Excellent penetrating properties- effective against intercellular Chlamydia & Rickettsia
    • *Used for UTIs, STDs, walking pneumonia (mycoplasma)
    • *Can cause superinfection - kills normal flora
    • *Can stain developing teeth
    • *Eyedrops for neonates

    • Tetracycline
    • Doxycycline
  21. Macrolides
    • INHIBITS PROTEIN SYNTHESIS
    • * Better for Gram (+) infections (dont penetrate outer cell membrane very well)
    • * Sits in tunnel between 30S & 50S subunits - inhibits protein systhesis
    • * Used for ppl with PCN allergies
    • * Bacteriostatic

    • Erythromycin
    • Zithromax (broad spectrum)
  22. Lincosamides
    • INHIBITS PROTEIN SYNTHESIS
    • * Broad spectrum - bacteriostatic
    • * Used for MRSA, anerobic bacteria, protists
    • * Semi-synthetis
    • * Can cause C. difficile overgrowth - causes pseudomembranous colitis

    Clindamycin
  23. Polymyxin B
    • INJURY TO PLASMA MEMBRANE
    • *plasma membrane looses its selective permeability
    • * can kill Gram (-) (pseudomonas)
    • * combined with neomycin or bacitracin in antibiotic ointment
  24. Rifamycins
    • DNA/ RNA SYNTHESIS INHIBITOR
    • *Block transcription of DNA (no mRNA, no protein)
    • * Anti TB drug - combined with INH to reduce chance of resistant stratins
    • * Able to penetrate macrophages (TB), abscesses, CSF

    Rifampicin - Rifampin
  25. Quinolones
    • DNA/ RNA SYNTHESIS INHIBITOR
    • *inhibit DNA gyrase - DNA cant unwind
    • * Broad stectrum - synthetic
    • * UTIs - IV drug for urosepsis
    • * not for children - affects cartilage growth and can cause spontaneous tendon rupture

    • Ciprofloxacin = Cipro
    • Levofloxacin = Levaquin
  26. Sulfonamides - Sulfa drugs
    • COMPETITIVE INHIBITOR
    • * Competitive inhibitor of PABA (para-aminobenzoic acid) - blocks folic acid synthesis from PABA - folic acid is necessary for nucleotide synthesis for DNA replication
    • * Broad spectrum - bacteriostatic

    1. Bactrim = TMP (trimethoprim) + SMZ (sulfamethoxazole) - synergistic

    • 2. Silvadene = silver + sulfadiazine
    • - used for burns - silver (heavy metal toxicity to bacteria -denatures proteins)
  27. How do antifungals work?
    Fungi are eukaryotes - hard to make durgs with "selective toxicity"

    • 1. affect sterols (ergosterol) in plasma membrane
    • 2. affect cell wall
    • 3. affect DNA/ RNA synthesis
    • 4. other
  28. Antifungals that affect ergosterol (a sterol) in the cell membrane
    • ANTIFUNGALS THAT EFFECT STEROLS
    • * effect ergosterol and effect seletive permeability
    • 1. Amphotericin B - (IV) for systemic fungal infections
    • - PO for oral thrush
    • - nephrotixic (kidney)

    • 2. Ketoconozole
    • - PO for systemic fungal infections
    • - used topically for athletes foot, ringwork, 2% prescrition shampoos
    • - hepatotoxic (liver)

    • 3. Miconazole = eg Monistat 7
    • - topical for candida vaginitis, athletes foot, ringworm
    • - used to prevent fungal growth on camera film

    • 4. Terbinafine - Lamisil
    • - treatment for dermatophytes (nail fungus)
  29. Other antifungal drugs:
    • Griseofulvin - Fulvicin
    • - PO for dermatophytes in/on skin, hair, nails
    • - block microtubole assembly in the mitotic spindle - cell not able to divide
    • - must bind to keratin to work
  30. How do anti-viral drugs work?
    • 60% of all infectious disease is caused by viruses
    • selective toxicity is difficult - virus lives in host cell

    • 1. Stop DNA replication - nucleotide analogues (fake nucleotides) block DNA polymerase function
    • 2. Reverse transcriptase inhibitors - AZT
    • 3. Protease inhibitors - blocks assembly
    • 4. Integrase inhibition - blocks provirus formation
    • 5. Fusion inhibition - blocks viral entry into cell
    • 6. Inhibits viral uncoating
  31. Viral Nucleotide Analogues
    Fake nucleotides - block DNA replication

    • 1. acyclovir = Zovirax - PO & ointment
    • - herpes simplex I & II, varicella (chicken pox, shingles), epstein barr virus (mono)

    2. lamivudine - for Hep B & HIV (also blocks reverse transcriptase)
  32. Reverse Transcriptase Inhibitors
    • AZT - zidubvidine - for HIV
    • - blocks reverse transcriptase - cant make DNA
  33. Drugs that Inhibit viral uncoating
    Stops virus from uncoating one inside the cell

    • 1. amantadine - for Influenza
    • *used to treat influenza, not prevent it - keeps virus from replicating


    • 2. Interferon - made by infected cells & prevents spread of virus to uninfected cells (keep virus from replication in uninfected cells)
    • - used to treat hep B & C, MS, viral cancers, infulenza
    • - can be toxic- liver, heart, kidney
  34. Antiprotazoal Drugs
    • 1. Chloroquine - quinine derivative
    • - #1 drug for malaria (plamodium infection)
    • - drug enters microbe with Host RBC & prevents microbe form detoxifying here → parasite death

    • 2. Metronidazole = Flagyl
    • *Damages DNA (disrupts double helix shape)
    • Rx Giardia - beaver fever - protazoa
    • Rx Trichomonas vaginalis
    • Also
    • Rx Chlamydia vaginitis -obligate intercellular bacteria
    • Rx anerobic bacteria - used for GI pre-op prophylaxis
    • & bowel perforations

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