Antimicrobials 1 and 2 Flashcards
Define antibiotic and antimicrobial
Antibiotic: technically a naturally produced chemical from a microorganism. Antibacterial: drugs to treat bacterial infections
Define bacteriostatic and bactericidal
Static stops growth so immune system can catch up. Cidal kill bacteria. Best for life-threatening or when immune systems broken.
Principles of Antimicrobial Therapy Flowchart.
Insert chart.
Betalactams
Only work when the cells are actively dividing
Penicillin pyramid
Penicillin most narrow, amoxicillin/ampicillin more, pipercillin most. Cloxacillin on the side only fights staph, some strep. Tunnels = add another drug to amoxicillin/pipercillin. Insert Picture.
General facts Cephalosporins
From mold. Blocks cross linking of peptidoglycan, activate autolytic enzymes. Gram -ve coverage increases with generation, gram +ve decreases. No Listeria, no Enterococcus, no coagulase negative staphylococci
Generations of cephalosporins
- Good gram +ve cocci, some gram -ve rod; 2. Good gram +ve cocci, more gram -ve; 3. Not great staph, good strep, even more gram -ve; 4. Good gram +ve, most gram -ve
Names of drugs in the generations of cephalosporins
1st: Cefazolin, cephalexin (po). 2nd: Cefuroxime, cefprozil. 3rd: (all T’s) Cefotaxime, ceftazidime, ceftriaxone, cefixime (po). 4th: cefepime
Monobactams
Aztreonams. No anaerobes covered.
Carbapenems
Imipenem and meropenem (fewer side effects) - cover almost all diseases.
Vancomycin
NOT A BETA LACTAM. Acts on early peptidoglycan wall synthesis
Bacitracin
NOT A BETA LACTAM. Acts by inhibiting the precursors from getting to the site of peptidoglycan wall synthesis. Only used as a cream/topical agent because of side effects
Summary of the drugs that affect cell wall
The cell wall active agents are the penicillins, the cephalosporins, the carbapenems, aztreonam and vancomycin. Penicillins – penicillin tree. Cephalosporins – ceph cycle. Aztreonam only gram negs. Carbapenems - gorillacillin. Vancomycin and bacitracin– only gram pos
Protein inhibitors
Need to be actively transported into cell - therefore don’t work well on anaerobes.
Aminoglycosides
Protein inhibitor. Gut gram negatives, bacteriocidal.
Macrolides/Erythromycins
Protein inhibitor. Mycoplama, chamydia, gram +ve, and respiratory gram -ve . Bacteriostatic.
Clindamycin
Protein inhibitor. Bacteriostatic. Common for dental and gyne. Gram positive aerobe and anaerobe
Chloramphenicol
Protein inhibitor. Bacteriostatic. Rarely used due to side effects - affect bone marrow and mitochondria.
Tetracycline, doxycycline, tigecyclin
Protein inhibitor. Bacteriostatic. Good coverage. Deposit on bones and teeth, can stain.
Linezolid
Protein inhibitor. Bacteriostatic. Acts on ribosome. Good for highly resistant gram +ve infections (superbugs)
Drugs that affect nucleic acid synthesis.
Work on proteins that affect nucleic acids ie ribosomes, gyrase, other enzymes, etc.
Quinolones
Inhibit enzymes for supercoiling (gyrase, etc). 1: rare. 2. Ciprofloxacin (urinary, diarrhea, gram +ve). 3. Levofloxain (pneumonia from community, mostly gram +, some gram -). 4. Gemifloxacin (powerful).
Metronidazole
Affect nucleic acid synthesis. Converted to active form by anaerobic or parasites. May be cancerous.
Rifampin
Inhibits RNA polymerase. Used in combination for mycobacteria. Prophylaxis against N meningitidis.
Antimetabolites
Binary fission requires cofactors like THF and folic acid. Antimetabolites block these.
TMP/SMX
Antimetabolites. No anaerobes. coverage good
Cytoplasmic membrane agents
Polymyxin - alters permeability; Good for gram -ve rods. Daptomycin - distrupts CM; reserved for highly resistant gram +ve cocci
How can bacteria become resistant?
Acquire genes via 3 mechanisms: Conjugation (plasmid). Bacteriophage transduction. Transformation (extracellular DNA)
What are the resistance mechanisms?
Block target, change target, fake (different metabolic pathway), attack (breakdown before it can bind), efflux pump
