Antimicrobials Flashcards
Antibiotics that are generally bacteriostatic
Chloramphenicol, Erythromycin/Macrolide, Clindamycin, Sulfonamide, Trimethoprim, Tetracycline, Tigecycline, Linezolid, Quinupristin/Dalfopristin
Antibiotics that are generally bactericidal
Vancomycin, Daptomycin, Fosfomycin, Aminoglycosides, Beta-lactams, Tedizolid, Levofloxacin, Rifampin, Metronidazole, Colistin
Mechanism of action for Penicillin, Cephalosporin, Carbapenem, Monobactam, Bacitracin
Inhibits enzymes for peptidoglycan synthesis (Cell wall synthesis inhibitors)
Mechanism of action for Vancomycin
Binds to peptidoglycan (Cell wall synthesis inhibitor) - Active against GP, MRSA
Mechanism of action for Daptomycin
Binds and disrupts cell membrane (Cell membrane synthesis inhibitor) - Active against GP
Mechanism of action for Colistin and Polymyxin
Binds and disrupts cell membrane (Cell membrane synthesis inhibitor) - Active against GN
Mechanism of action for Aminoglycosides and Tigecycline
Inhibits 30s ribosomal subunit (Protein synthesis inhibitors) - Active against GP and GN
Mechanism of action for Chloramphenicol, Macrolides, and Clindamycin
Inhibits 50s ribosomal subunit (Protein synthesis inhibitors) - Active against GP and GN
Mechanism of action for Linezolid, Tedizolid, and Streptogramins
Inhibits 50s ribosomal subunit (Protein synthesis inhibitors) - Active against GP
Mechanism of action for Fluoroquinolones and Nalidixic acid
Inhibits DNA synthesis (Nucleic acid synthesis inhibitors) - Active against GP and GN
Mechanism of action for Nitrofurantoin
Damages DNA directly (Nucleic acid synthesis inhibitor) - Active against GP and GN (UTI only)
Mechanism of action for Sulfonamides and Trimethoprim
Interferes with folic acid pathway - Active against GP and many GN bacteria
Mechanism of action for Rifampin
Inhibits RNA synthesis - Active against GP and Neisseria meningitidis
Antibiotics effective only against GP bacteria
Vancomycin (except VRE, Lactobacillus, Leuconostoc, Pediococcus), Daptomycin, Linezolid, Tedizolid, Streptogramins
Antibiotics effective only against GN bacteria
Colistin, Polymyxin
Antibiotics effective against both GP and GN bacteria
Penicillin, Cephalosporin, Carbapenem, Monobactam, Bacitracin, Aminoglycosides, Tigecycline, Chloramphenicol, Macrolides, Clindamycin, Tetracycline, Fluoroquinolones, Sulfonamide, Trimethoprim
Vancomycin resistance in GN bacteria
All GN bacteria are resistant except Chryseobacterium, Moraxella, and Acinetobacter
Colistin and Polymyxin resistance in GP bacteria
Most GP are resistant, while most GN are susceptible
Reduced susceptibility of an organism to a particular antimicrobial.
Biologic resistance
Occurs when an antimicrobial can no longer be used clinically against a certain bacteria.
Clinical resistance
Resistance due to the microorganism’s normal genetic, structural, or physiological state.
Intrinsic resistance
Resistance resulting from altered cellular physiology and structure caused by genetic changes.
Acquired resistance
Intrinsic resistance: GP bacteria
Aztreonam
Intrinsic resistance: GN bacteria, Lactobacilli, Leuconostoc
Vancomycin
Intrinsic resistance: Pseudomonas aeruginosa
SXT, tetracycline, chloramphenicol
Intrinsic resistance: Stenotrophomonas maltophilia
Imipenem
Intrinsic resistance: Klebsiella
Ampicillin
Intrinsic resistance: Enterococci
Aminoglycoside, Cephalosporin
Intrinsic resistance: Anaerobic bacteria
Aminoglycoside
Intrinsic resistance: Aerobic bacteria
Metronidazole
Mechanism of resistance: Enzymatic destruction
Beta-lactamase destroys the β-lactam ring of antibiotics; e.g., Staphylococcus resistance to penicillin; Enterobacterales and P. aeruginosa resistance to β-lactam drugs.
Mechanism of resistance: Enzymatic modification
Modifying enzymes alter antibiotic binding sites, causing GP and GN resistance to aminoglycosides.
Mechanism of resistance: Altered target in bacteria
Mutation in original PBP to PBP2a; e.g., MRSA (PBP -> PBP2a), VRE, VRSA.
Mechanism of resistance: Cell wall alteration
Structural changes lead to resistance; e.g., S. pneumoniae and Viridans resistance to β-lactam drugs.
Mechanism of resistance: Decreased antibiotic uptake
Porin channel reduction blocks antibiotic entry; e.g., P. aeruginosa resistance to imipenem, GN resistance to aminoglycosides.
Mechanism of resistance: Efflux of antibiotic
Bacteria pump the drug out before it binds to the target; e.g., Staphylococcus and Streptococcus resistance to macrolides.