Flashcards in Antibacterials Deck (77):
Inhibit PBPs, which catalyze cell wall crosslinks. Competitive and irreversible.
1. B-lactamase (most prevalent).
2. Altered PBP (MRSA).
Allergic reactions: Anaphylaxis, rash.
Penicillin G and V:
-GM+ anaerobes (B-lactamase negative Strep).
-Neisseria meningitidis (behind Ceftriaxone).
-B-lactamase-negative GM+ (Streptococcus, listeria).
-First-line treatment for otitis media.
-Same as amoxicillin, plus treats meningitis (Neisseria, Listeria), GI infections.
-Broad GM- effectiveness, including pseudomonas aeruginosa.
-Often used with a B-lactamase inhibitor to hit anaerobes.
-Broad GM- effectiveness, including pseudomonas and klebsiella (ticarcillin-resistant)
-Often used with a B-lactamase inhibitor.
2 B-lactamase inhibitors:
1. Clavulanic acid.
Cephalosporins spectrum of activity:
1st generation: best for GM+
2nd generation: more GM- activity.
3rd generation: best for GM -
-Surgical prophylaxis against skin flora.
-Oral form of Cefazolin.
-Only 2nd gen to penetrate CSF.
-Best of 2nd gen against Haemophilus.
-Cefuroxime plus added benefits against anaerobes such as Bacteroides.
-1st line against gonorrhea, meningitis (Neisseria).
-Active against Pseudomonas.
-Similar spectrum to Ceftazidime, except more resistant to type I B-lactamases.
-Empirical treatment of serious inpatient infections.
Imipenem use and side effects:
-Resistant to many B-lactamases, including ESBLs.
-Not effective against MRSA.
-Give with cilastatin, a renal peptidase inhibitor.
-Use if mixed or ill-defined infection, those not responsive to other drugs.
Side effects: Hypersensitivity, seizures, dizziness, confusion, GI effects.
-Used against GM- aerobic rods.
-Resistant to many B-lactamases.
-Can be used in those with known hypersensitivities to penicillins.
Side effects: seizures, GI effects, anaphylaxis, transient EKG changes.
MOA: Inhibits cell-wall synthesis: by interfering with cross-linking and elongation of the peptidoglycan chains.
-First line against HA-MRSA.
-Severe C diff infections (behind metronidazole).
-“Red neck” syndrome.
Inactivates enolpyruvyl transferase, an early stage cell wall synthesis enzyme.
-Uncomplicated UTIs caused by E. coli, enterococcus.
Interferes with lipid carrier that exports early cell wall components through the cell membrane.
Topical agent against GM+
Cationic detergents that bind LPS in the outer membrane of GM-
Topical agent against GM-, pseudomonas.
Binds to bacterial cytoplasmic membrane, causing rapid membrane depolarization.
-Complicated skin infections (Staph. Aureus, streptococcus, enterococcus).
Quinolones MOA & MOR:
MOA: Inhibits bacterial DNA gyrase, thus interfering with replication and repair.
MOR: 1. Altered DNA gyrase.
2. Decreased permeability.
3. Combo of the two.
Quinolones SEs and contraindications:
-Contraindicated in those with seizure disorders, pregnancy, children.
-Athropathy, tendon rupture.
Name the quinolones:
UTIs (achieve therapeutic concentrations only in the UG region).
UTIs, infectious diarrhea, skin infections, bone and joint infections, chlamydia.
-Better GM+ spectrum than most quinolones.
-Respiratory infections (NOT strep throat).
-CA pneumonia, bacterial bronchitis.
Nitrofurantoin MOA, use, SEs:
MOA: Nitroreductase enzyme converts drug to reactive compounds which can damage DNA.
Use: Lower UTIs.
SEs: -Peripheral neuropathy.
-Pulmonary fibrosis in elderly.
Inhibitor of RNAP, thereby inhibiting RNA synthesis.
-Primarily for treatment of pulmonary TB.
-Prophylaxis of meningococcal meningitis, haemophilus influenza.
-Part of combination therapy for leprosy.
-Orange urine, tears, sweat.
-Strongly induces CYP3A.
-3rd line for C diff (behind metronidazole, vancomycin).
-Only hits clostridium, so useful for allowing patient to restore normal gut flora.
-Less recurrence of C diff than vanco and metronidazole.
Inhibitor of RNAP, thereby inhibiting RNA synthesis.
-C diff enterocolitis.
-Combination therapy for H. pylori.
Anaerobes reduce the nitro group, resulting product disrupts DNA.
-Long-term treatment: leukopenia, neutropenia.
-Bacterial and fungal superinfections (Candida).
Transported into bacteria by an energy-requiring aerobic process. Binds to several ribosomal sites, stopping initiation, causes premature release of ribosome from mRNA, and mRNA misreading.
-More effective against GM- than GM+, but when using against GM+, use with quinolone or cell wall inhibitor.
-Use only against serious infections because of toxicity.
--Post-antibiotic effect: sustained activity for several hours after aminoglycoside concentration has dropped below effective levels. Allows for less frequent dosing.
--Do not mix B-lactams with aminoglycosides in vitro – will inactivate the drug.
Name the aminoglycosides:
3. Amikacin (most broad spec)
Name the tetracyclines:
Blocks protein synthesis by binding to the 30S ribosomal subunit, preventing attachment of aminoacyl-tRNA to the acceptor site.
1. Efflux pumps.
-Preferred agents for rickettsia, chlamydia, Mycoplasma, Ureaplasma, Borrelia.
-Ca++ inhibits absorption.
Same as the tetracyclines, but binds additional sites on ribosomes.
-Used against many GM+, including MRSA.
-A few GM-, but NOT pseudomonas.
Blocks protein synthesis: Inteferes with binding of aminoacyl-tRNA to 50S subunit, and inhibits peptide bond formation.
Broad spec – only use in serious cases.
-Alternative agent for meningitis, brain abscesses.
-Bone marrow depression, can progress to a fatal aplastic anemia.
-Grey baby syndrome.
Block protein synthesis by binding to the 50S ribosomal subunit, blocking the translocation step.
-Increases risk of arrhythmias and cardiac arrest (QT prolongation).
-Enhances GI motility.
-Primarily against GM+ (Staph and Strep)
-Also against Chlamydia, mycoplasma, bordetella, campylobacter.
-Interferes with CYP3A metabolism of other drugs.
-Better kinetics than erythromycin (less frequent dosing).
-Less GI motility.
-Somewhat wider spectrum.
-Uses are same as erythromycin
-Also part of combination therapy for H pylori.
-Also used for MAC treatment, prophylaxis.
- Gonorrhea (ceftriaxone + azithromycin or doxycycline).
Same as macrolides, but not a macrolide.
-Inhibits most GM+ cocci, and many anaerobes, incl. Bacteroides fragilis.
-Suppresses bacterial toxin production (Strep and Staph).
Blocks protein synthesis by binding to the 50S ribosomal subunit, interfering with the formation of 70S initiation complex.
-1st line against CA-MRSA.
-Bone marrow depression.
-Non-selective inhibitor of MAO (avoid foods with tyramine).
Inhibit folate synthesis in bacteria by competitive inhibition of dihydropteroate synthase.
-Renal damage from crystalluria.
-Inhibit CYP2C9 – potentiates action of other drugs (Warfarin).
UTIs, bacillary dysentery, typhoid fever.
Use on burn wounds.
Given in conjunction with sulfamethoxazole – combined effects are bactericidal.
Used for UTIs, URIs and otitis media.
-Also for Pneumocystis jiroveci.
Inhibit folate synthesis in bacteria by competitively inhibiting dihydrofolate reductase.