1. Penicillin Types (PCN) B-Lactams
    • Natural Penicillins
    • Antistaphylococcal penicillins
    • Extendend spectrum penicillins:
    • 1. Aminopenicillins
    • 2. Carboxypenicillins
    • 3. Ureidopenicillins
  2. Bacteria: Gram Positive
    thick peptidoglycan cell wall
  3. Bacteria: Gram Negative: hard for antibiotics to penetrate
    • Outer membrane: extra lipopolysaccharide membrane surrounding the cell wall and includes porins channels which allow entry into cell
    • Inner membrane: thin peptidoglycan layer which makes up the cell wall
  4. Bacteria Cell Wall
    is composed of cross linked polysaccarides.
  5. Antibiotics/B Lactams
    cause a change of PBP or an alteration

    • cause the penicillin binding proteins to block/prevent or STOP crosslinking or formation of a rigid bacterica cell wall from occuring. No crosslinking of bacteria cell wall=bateria death. Crosslinking=viable bacterial
    • B-Lactams prevent development of a normal bacterial cell wall
  6. Bacteria Cell Wall Crosslinking
    bacteria live, bacteria strong, bacteria spread
  7. Bacteria Cell wall NO crosslinking
    weak bacteria, death of bacteria
  8. Different Antibiotics work on
    different penicillin binding proteins (PBP) and prevent cell wall synthesis
  9. Penicillin Binding Proteins (PBP)
    Are enzymes that break off a part of the polysaccaride wall to promote cross linking. There are thousands of different PBP. If crosslinking occurs then bacteria are viable and the infection spreads. PBP are different in gram+ bacteria, gram- bacteria and anaerobic bacteria
  10. B-Lactam is only effective if
    the bacteria is in the growing/active stage

    bacteria need to be actively multiplying
  11. Bacteria are very smart and have figured out over the years to
    change their PBP shape and therefore lower their affinity for B-lactams or lower their affininty to PCN. Now betalactam will no longer be effective. Now it will no longer prevent that crosslinking

    Bacteria talk, they will share their knowledge of resistence mechanisms.
  12. MOA for Bacterial Resistance to B-Lactams
    1. change shape of PBP. This causes B-Lactams to no longer be effective

    2. Enzyme B-Lactamase breaks the B-Lactam ring. The bacteria produce this enzyme. If this ring is broken we lose our antibacterial activity. Very common

    3. Gram- bacteria change the structure of their porins. So the antibiotic can no longer get through to the cell wall. this is called Decreased Antibiotic Permeabitity. Impaired B-lactam penetration. If antibiotics dont get to the cell wall they will have no effect on it.

    4. Efflux Pump: bacteria has this pump. When antibiobics do get into the cell wall the bacteria just "PUMP" the antibiotic back out! This reduces the amount of intracellualar drug and there is never a strong enough concentration of antibiotic in the cell wall to have an effect.
  13. B-Lactamase Inhibitors: prevents breaking of bond on the b-Lactam structure
    combat resistance issues.
  14. Natural PCN
    • PCN G-IV
    • PCN VK-PO oral
    • Benzathine PCN-IM: used to treat SYPHILLIS. SYPHILLIS is a slow grwoing bacteria slowly absorbed, long acting
    • Procaine PCN-IM: not rx very often. slowly absorbed, prolonged low concentrations (weeks), contains local anesthetic
  15. Natural PCN MOA: overall limited/focused
    work on gram+. work well on strep but not the best for staph, limited to gram-
  16. Antistaphylcoccal PCN: great choice! most potent to tx staph and strep, NOT MRSA
    PCN was developed and we were using it. The staph got smart and started producing penicilinase which inactivated PCN
  17. Aminopenicillins
Card Set
Pharmacology Antibiotics