Antibiotics Flashcards
Penicillin
(ß-lactam)
Mechanism: Binds PBP transacetylase, prevents peptidoglycan crosslinking.
Resistance from: (1) PBP mutations (as in MRSA),
and (2) ß-lactamase (can be blocked with clavulanic acid, tazobactam, or sulbactam).
Used for: S. pyogenes pharyngitis.
Amoxicillin
(ß-lactam)
Mechanism: Binds PBP transacetylase, preventing peptidoglycan crosslinking.
Resistance from: (1) PBP mutations (as in MRSA),
and (2) ß-lactamase (can be blocked with clavulanic acid, tazobactam, or sulbactam).
Used for: S. pyogenes pharyngitis.
Cephalosporin
(ß-lactam)
Mechanism: Binds PBP transacetylase, preventing peptidoglycan crosslinking.
Resistance from: (1) PBP mutations (as in MRSA),
and (2) ß-lactamase (can be blocked with clavulanic acid, tazobactam, or sulbactam).
Carbapenem
(ß-lactam)
Mechanism: Binds PBP transacetylase, preventing peptidoglycan crosslinking.
Resistance from: (1) PBP mutations (as in MRSA),
and (2) ß-lactamase (can be blocked with clavulanic acid, tazobactam, or sulbactam).
Monobactam
(ß-lactam)
Mechanism: Binds PBP transacetylase, preventing peptidoglycan crosslinking.
Resistance from: (1) PBP mutations (as in MRSA),
and (2) ß-lactamase (can be blocked with clavulanic acid, tazobactam, or sulbactam).
Cycloserine
Mechanism: Competes with D-ala for crosslinking.
Used for: Second-line TB.
Bacitracin
(Neosporin)
Mechanism: Binds pyrophosphate on lipid carriers, prevents peptidoglycan recycling.
Used for: Topical antiseptic. Also diagnostic use for GAS.
Daptomycin
(Cell envelope antibiotic)
Mechanism: Disrupts cell membrane.
Used for: Gram positive bacteria, narrow spectrum.
Polymyxins
(Cell envelope antibiotic)
Mechanism: Disrupts outer cell membrane.
Used for: Gram negative bacteria.
Cephalosporin
(ß-lactam)
Mechanism: Binds PBP transacetylase, prevents peptidoglycan crosslinking.
Resistance from: (1) PBP mutations (as in MRSA),
and (2) ß-lactamase (can be blocked with clavulanic acid, tazobactam, or sulbactam).
Carbapenem
(ß-lactam)
Mechanism: Binds PBP transacetylase, prevents peptidoglycan crosslinking.
Resistance from: (1) PBP mutations (as in MRSA),
and (2) ß-lactamase (can be blocked with clavulanic acid, tazobactam, or sulbactam).
Monobactam
(ß-lactam)
Mechanism: Binds PBP transacetylase, prevents peptidoglycan crosslinking.
Resistance from: (1) PBP mutations (as in MRSA),
and (2) ß-lactamase (can be blocked with clavulanic acid, tazobactam, or sulbactam).
Vancomycin
Mechanism: Binds D-ala-D-ala, prevents transpeptidation and transglycosylation.
Resistance: Evolves D-ala-D-lac (as in VRE, VRSA).
Used for: Gram positive bacteria only
Polymyxins
(Cell envelope antibiotic)
Mechanism: Binds LPS, disrupts outer cell membrane.
Used for: Gram negative bacteria.
Doxycycline
(a tetracycline)
Mechanism: Binds 30S, prevents tRNA binding.
Resistance: Tetracycline pump.
Adverse effects: teeth discoloration, bone malformation during development.
Uses: Overused; many bacteria are resistant now.
Minocycline
(a tetracycline)
Mechanism: Binds 30S, prevents tRNA binding.
Resistance: Tetracycline pump.
Adverse effects: teeth discoloration, bone malformation during development.
Uses: Overused; many bacteria are resistant now.
Gentamicin
(an aminoglycoside)
Mechanism: Binds 30S, reduces RNAP processivity.
Resistance: Drug modification.
Adverse effects: ototoxicity, nephrotoxicity.
Uses: Hard-to-kill Gram negative bacteria, such as Pseudomonas aeruginosa.
Amikacin
(an aminoglycoside)
Mechanism: Binds 30S, reduces RNAP processivity.
Resistance: Drug modification.
Adverse effects: ototoxicity, nephrotoxicity.
Uses: Hard-to-kill Gram negative bacteria, such as Pseudomonas aeruginosa.
Kanamycin
(an aminoglycoside)
Mechanism: Binds 30S, reduces RNAP processivity.
Resistance: Drug modification.
Adverse effects: ototoxicity, nephrotoxicity.
Uses: Hard-to-kill Gram negative bacteria, such as Pseudomonas aeruginosa.
Tobramycin
(an aminoglycoside)
Mechanism: Binds 30S, reduces RNAP processivity.
Resistance: Drug modification.
Adverse effects: ototoxicity, nephrotoxicity.
Uses: Hard-to-kill Gram negative bacteria, such as Pseudomonas aeruginosa.
Erythromycin
(a macrolide)
Mechanism: Binds 50S, prevents elongation.
Resistance: (1) Efflux pumps, and (2) ribosomal methylation by erm methylase.
Uses: Gram positive bacteria, including B. pertussis (whooping cough).
Azithromycin
(a macrolide)
Mechanism: Binds 50S, prevents elongation.
Resistance: (1) Efflux pumps, and (2) ribosomal methylation by erm methylase.
Uses: Gram positive bacteria.
Clarithromycin
(a macrolide)
Mechanism: Binds 50S, prevents elongation.
Resistance: (1) Efflux pumps, and (2) ribosomal methylation by erm methylase.
Uses: Gram positive bacteria.
Chloramphenicol
Mechanism: Binds 50S, prevents elongation.
Resistance: Drug modification (chloramphenicol acetyltransferase).
Adverse effects: Aplastic anemia.
Uses: Avoid if possible, as AEs are serious.
Clarithromycin
(a macrolide)
Mechanism: Binds 50S, prevents elongation.
Resistance: (1) Efflux pumps, and (2) ribosomal methylation by erm methylase.
Uses: Gram positive bacteria.
Clindamycin
Mechanism: Binds 50S, prevents elongation.
Resistance: Ribosomal methylation by erm methylase.
Side effects: so effective that C. difficile can populate!
Uses: MRSA (community acquired), S. aureus (toxin-producing), systemic Strep infections.
Chloramphenicol
Mechanism: Binds 50S, prevents elongation.
Resistance: Drug modification (chloramphenicol acetyltransferase).
Adverse effects: Aplastic anemia.
Uses: Avoid if possible, as AEs are serious.
Clindamycin
Mechanism: Binds 50S, prevents elongation.
Resistance: Ribosomal methylation by erm methylase.
Uses: MRSA (community acquired), S. aureus (toxin-producing), systemic Strep infections.
Linezolid
Mechanism: Binds 23S rRNA of 50S, prevents formation of 70S.
Mechanism: Point mutations to prevent binding.
Uses: Gram positive bacteria (esp. S. aureus, S. pyogenes, S. agalactiae).
Linezolid
Mechanism: Binds 23S rRNA of 50S, prevents formation of 70S.
Mechanism: Point mutations to prevent binding.
Uses: Gram positive bacteria (esp. S. aureus, S. pyogenes, S. agalactiae).
Nalidixic acid
(a quinolone; a first-generation DNA replication inhibitor)
Mechanism: Binds DNA gyrase (topoisomerase), prevents replication and repair.
Resistance: (1) Efflux pumps, and (2) point mutations in gyrase.
Norloxacin
(a fluoroquinolone; a second-generation DNA replication inhibitor)
Mechanism: Binds DNA gyrase (topoisomerase), prevents replication and repair.
Resistance: (1) Efflux pumps, and (2) point mutations in gyrase.
Ciprofloxacin
(a fluoroquinolone; a second-generation DNA replication inhibitor)
Mechanism: Binds DNA gyrase (topoisomerase), prevents replication and repair.
Resistance: (1) Efflux pumps, and (2) point mutations in gyrase.
Ciprofloxacin
(a fluoroquinolone; a second-generation DNA replication inhibitor)
Mechanism: Binds DNA gyrase (topoisomerase), prevents replication and repair.
Resistance: (1) Efflux pumps, and (2) point mutations in gyrase.
Metronidazole
Mechanism: Makes free radicals in aerobic environments.
Used for: Anaerobes, such as C. difficile.
Rafampin
(an RNA synthesis inhibitor)
Mechanism: Binds ß subunit of RNAP.
Resistance: Mutation of ß subunit of RNAP.
Fidaxomicin
(an RNA synthesis inhibitor)
Mechanism: Binds ß subunit of RNAP.
Resistance: Mutation of ß subunit of RNAP.
Sulfonamide
(an antimetabolite)
Mechanism: Inhibits DHPS (dihydropteroate synthetase).
Resistance: Use of another pathway.
Trimethoprim
(an antimetabolite)
Mechanism: Inhibits DHFR.
Resistance: Use of another pathway.
