Antimicrobials Flashcards
Penicillin V
Prototype B lactam antibiotic–Oral form
MOA: binds PBPs and blocks transpeptidase crosslinking
Uses: mostly gram positive (s. Pneumo, s. Pyogenes, actinomyces); Also used for N? Meningitidis and T. pallidum. Bactericidal for gram positive cocci, gram positive rods, gram negative cocci, and spirochetes. Penicillinase sensitive.
TOXICITY: hypersensitivity reactions, hemolytic anemia.
RESISTANCE: penicillinase in bacteria (a type of B lactamase) cleaves B lactam ring
Penicillin G
Prototype B lactam antibiotic–IV and IM form
MOA: binds PBPs and blocks transpeptidase crosslinking
Uses: mostly gram positive (s. Pneumo, s. Pyogenes, actinomyces); Also used for N? Meningitidis and T. pallidum. Bactericidal for gram positive cocci, gram positive rods, gram negative cocci, and spirochetes. Penicillinase sensitive.
TOXICITY: hypersensitivity reactions, hemolytic anemia.
RESISTANCE: penicillinase in bacteria (a type of B lactamase) cleaves B lactam ring
Ampicillin
Penicillinase-sensitive penicillin
MOA: same as penicillin. Wider spectrum; penicillinase sensitive. Also combine with clavulanic acid to protect against B-lactamase.
USES: extended-spectrum penicillin–Haemophilus influenzae, E. Coli, Listeria monocytogenes, Proteus mirabilis, Salmonella, Shigella, enterococci (ampicillin/amoxicillin HELPSS kill enterococci)
TOXICITY: hypersensitivity reactions; rash; pseudo membranous colitis
RESISTANCE: penicillinase in bacteria (a type of B lactamase) cleaves B-lactam ring
Oxacillin
Penicillinase-resistant penicillin
MOA: same as penicillin. Narrow spectrum; penicillinase resistant because bulky R group blocks access of B lactamase to B lactam ring.
USE: S. aureus (except MRSA; resistant because of altered PBP target site)
TOXICITY: hypersensitivity reactions, interstitial nephritis
Pipercillin
Antipsuedomonal
MOA: same as penicillin. Extended spectrum.
USES: Pseudomonas spp. And gram negative rods; susceptible to penicillinase; use with B lactamase inhibitors.
TOXICITY: hypersensitivity reactions
Cephalosporins
Inhibits peptidoglycan cross-linking; less susceptible to penicillinase than penicillin
1st generation: cefazolin, cephalexin
2nd generation: cefaclor, cefprozi, cefoxitin
3rd generation: cefpodoxime, cefotaxime, ceftriaxone
4th generation: cefepime
1st generation cephalosporins
Cefazolin, cephalexin
PEcK: Proteus mirabilis, E. coli, Klebsiella pneumoniae
Don’t penetrate CNS
2nd generation cephalosporins
Cefaclor, cefprozi, cefoxitin; extended gram negative spectrum
HEN PEcKS: Haemophilus influenzae, Enterobacter, Neisseria, Proteus, E. Coli, Klebsiella, Serratia
3rd generation cephalosporins
Cefpodoxime, cefotaxime, ceftriaxone
Serious gram negative infections resistant to other beta lactams
Penetrates the CNS-meningitis, gonorrhea, pseudomonas
Less effective against gram positive than 1st
4e generation cephalosporins
Cefepime
Increased activity against pseudomonas and gram positive
Enhanced resistance to beta lactamase
Crosses the BBB
Imipenem
Cabapenem
MOA: broad-spectrum, B-lactamase-resistant capbapenem. Inhibit cell wall synthesis. Always administered with cilastatin (inhibitor of renal dehydropeptidase I) to decreased inactivation of drug in renal tubules.
USES: gram positive cocci, gram negative rods, and anaerobes. Wide spectrum, but significant side effects limit use to life threatening infections or after other drugs have failed.
TOXICITY: GI distress, skin rash, and CNS toxicity (seizures) at high plasma levels.
Vancomycin
MOA: inhibits cell wall peptidoglycan formation by binding D-ala D-ala portion of cell wall precursors. Bacteriocidal.
USES: gram positive only–serious, multidrug-resistant organisms, including MRSA, enterococci, and Clostridium difficile (oral dose for pseudomembranous colitis)
TOXICITY: well tolerated in general–but NOT trouble free. Nephrotoxicity, ototoxicity, thrombophlebitis, diffuse flushing–red many syndrome (can largely prevent by pretreatment with antihistamines and slow infusion rate)
RESISTANCE: occurs in bacterial via amino acid modification of D-ala D-ala to D-ala D-lac
Tobramycin
Aminoglycoside–30S inhibitor
MOA: bactericidal; inhibits formation of inititation complex and causes misreading of mRNA. Also blocks translocation. Requires O2 for uptake; therefore ineffective against anaerobes.
USES: severe, gram negative rod infections. Synergistic with B lactam antibiotics.
TOXICITY: nephrotoxicity, neuromuscular blockade, ototoxicity (especially when used with loop diuretics), teratogenic.
RESISTANCE: bacterial transferase enzymes inactivate the drug by acetylation, phosphorylation, or adenylation.
Doxycycline
MOA: bacteriostatic; binds 30s and prevents attachment of aminoacyl-tRNA; limited CNS penetration. Doxycycline is fecally eliminated and can be used in patients with renal failure. Do not take with milk (calcium), antacids (calcium or magnesium), or iron-containing preparations because divalent cations inhibit absorption in gut.
USES: Borrelia burgdorferi, M pneumoniae. Drug’s ability to accumulate intracellularly makes it very effective against Rickettsia and Chlamydia. Also used to treat acne.
TOXICITY: GI distress, discoloration of Teeth and inhibition of bone growth in children, photosensitivity. Contraindicated in pregnancy.
RESISTANCE: decreased uptake or increased efflux out of bacterial cells by plasmid-encoded transport pumps.
Erythromycin
Macrolide
MOA: binds 50S subunit and inhibits translocation. Bacteriostatic.
Uses: atypical pneumonias-mycoplasma, chlamydia, legionella, STDs (chlamydia), gram positive cocci (strep if allergic to penicillin)
TOXICITY: GI motility issues, arrhythmia caused by prolonged QT, Canute cholestatic hepatitis, rash, eosinophilia. Increases serum concentration of theophyllines, oral anticoagulants.
RESISTANCE: methylation of 23s rRNA-binding site prevents binding of drug.
Clindamycin
MOA: blocks peptide transfer (translocation) at 50s ribosomal subunit. Bacteriostatic.
USES: anaerobic infections (e.g. Bacteroides spp., Clostridium perfringens) in aspiration pneumonia, lung abscesses, and oral infections. Also effective against invasive Group A strep infection. **treats anaerobes above the diaphragm vs metronidazole
TOXICITY: pseudomembranous colitis (C. Difficile overgrowth), fever, diarrhea
Linezolid
Oxazolidinone
MOA: inhibits protein synthesis by binding to 50S subunit and preventing formation of the initiation complex.
USES: gram positive species including MRSA and VRE
TOXICITY: bone marrow suppression (especially thrombocytopenia), peripheral neuropathy, serotonin syndrome
RESISTANCE: point mutation of ribosomal RNA
Sulfamethoxazole
Sulfonamide
MOA: inhibits folate synthesis. Para-aminobenzoic acid (PABA) antimetabolites inhibit dihydropteroate synthase. Bacteriostatic.
Uses: gram positive, gram negative, Nocardia, Chlamydia. Triple sulfas or SMX for simple UTI.
TOXICITY: hypersensitivity reactions, hemolysis if G6PD deficient, nephrotoxicity (Tubulointerstitial nephritis), photosensitivity, kernicterus in infants, displace other drugs from albumin (e.g. Warfarin)
RESISTANCE: altered enzyme (bacterial dihydropteroate synthase), decreased uptake, or increased PABA synthesis
Trimethoprim
MOA: Inhibitor of dihydrofolate reductase. Bacteriostatic.
USES: used in combination with sulfonamides, causing sequential block of folate synthesis. Combination used for UTIs, shigella, salmonella, pneumocystis jirovecii pneumonia treatment and prophylaxis, toxoplasmosis prophylaxis.
TOXICITY: megaloblastic anemia, thrombocytopenia, leukopenia
Ciprofloxacin
fluoroquinolone
MOA: inhibits DNA gyrate (topoisomerase II) and topoisomerase IV. bactericidal. Must not be taken with antacids.
Uses: gram negative rods of urinary and GI tracts, Neisseria, some gram positive organisms
TOXICITY: GI upset, super infections, skin rashes, headache, dizziness. Less commonly, can cause tendonitis, tendon rupture, leg cramps, and myalgias. Contraindicated in pregnancy, nursing mothers, and children under 18 due to possible damage to cartilage. Some may cause prolonged QT interval. May cause tendon rupture in people over 60y and in patients taking prednisone.
RESISTANCE: chromosome-encoded mutation in DNA gyrase, plasmid-mediated resistance, efflux pumps.
Metronidazole
MOA: Forms free radical toxic metabolites in bacterial cell that Damage DNA. Bactericidal, antiprotozoal.
USES: treats GET GAP–Giardia, Entamoeba, Trichomonas, Gardnerella vaginalis, Anaerobes (Bacteroides, C. Difficile). Used with a proton pump inhibitor and clarithromycin for “triple therapy” against H. Pylori.
TOXICITY: disulfiram-like reaction (severe flushing, tachycardia, hypotension) with alcohol (thought to be due to its inhibition of alcohol oxidizing enzymes–>accumulation of acetaldehyde); headache, metallic taste
Amoxicillin
Penicillinase-sensitive penicillin
MOA: same as penicillin. Wider spectrum; penicillinase sensitive. Also combine with clavulanic acid to protect against B-lactamase.
USES: extended-spectrum penicillin–Haemophilus influenzae, E. Coli, Listeria monocytogenes, Proteus mirabilis, Salmonella, Shigella, enterococci (ampicillin/amoxicillin HELPSS kill enterococci)
TOXICITY: hypersensitivity reactions; rash; pseudo membranous colitis
RESISTANCE: penicillinase in bacteria (a type of B lactamase) cleaves B-lactam ring
Nafcillin
Penicillinase-resistant penicillin
MOA: same as penicillin. Narrow spectrum; penicillinase resistant because bulky R group blocks access of B lactamase to B lactam ring.
USE: S. aureus (except MRSA; resistant because of altered PBP target site)
TOXICITY: hypersensitivity reactions, interstitial nephritis
Dicloxacillin
Penicillinase-resistant penicillin
MOA: same as penicillin. Narrow spectrum; penicillinase resistant because bulky R group blocks access of B lactamase to B lactam ring.
USE: S. aureus (except MRSA; resistant because of altered PBP target site)
TOXICITY: hypersensitivity reactions, interstitial nephritis
Ticarcillin
Antipsuedomonal
MOA: same as penicillin. Extended spectrum.
USES: Pseudomonas spp. And gram negative rods; susceptible to penicillinase; use with B lactamase inhibitors.
TOXICITY: hypersensitivity reactions
Clavulanic acid
B-lactamase inhibitor. Often added to penicillin antibiotics to proct the antibiotic from destruction by B-lactamase (penicillinase)
Sulbactam
B-lactamase inhibitor. Often added to penicillin antibiotics to proct the antibiotic from destruction by B-lactamase (penicillinase)
Tazobactam
B-lactamase inhibitor. Often added to penicillin antibiotics to proct the antibiotic from destruction by B-lactamase (penicillinase)
Cefazolin
1st generation cephalosporin
MOA: B-lactam drug that inhibits cell wall synthesis but are less susceptible to penicillinases. Bacteriocidal.
USES: PEcK (gram positive cocci)–Proteus mirabilis, E. coli, Klebsiella pneumoniae. Cefazolin used prior to surgery to prevent S. aureus wound infections
TOXICITY: hypersensitivity reactions, autoimmune hemolytic anemia, disulfiram-like reaction (inhibits acetaldehyde dehydrogenase and causes hangover symptoms, severe flushing hypotension, tachycardia with alcohol). Exhibits cross reactivity with penicillins. Increases nephrotoxicity of aminoglycosides.
Cephalexin
1st generation cephalosporin
MOA: B-lactam drug that inhibits cell wall synthesis but are less susceptible to penicillinases. Bacteriocidal.
USES: PEcK (gram positive cocci)–Proteus mirabilis, E. coli, Klebsiella pneumoniae.
TOXICITY: 1st generation cephalosporin
MOA: B-lactam drug that inhibits cell wall synthesis but are less susceptible to penicillinases. Bacteriocidal.
USES: PEcK (gram positive cocci)–Proteus mirabilis, E. coli, Klebsiella pneumoniae. Cefazolin used prior to surgery to prevent S. aureus wound infections
TOXICITY: hypersensitivity reactions, autoimmune hemolytic anemia, disulfiram-like reaction (inhibits acetaldehyde dehydrogenase and causes hangover symptoms, severe flushing hypotension, tachycardia with alcohol). Exhibits cross reactivity with penicillins. Increases nephrotoxicity of aminoglycosides.
Cefoxitin
2nd generation cephalosporin
MOA: B-lactam drug that inhibits cell wall synthesis but are less susceptible to penicillinases. Bacteriocidal.
USES: HEN PEcKS (gram positive cocci)–Haemophilus influenzae, Enterobacter aerogenes, Neisseria spp., Proteus mirabilis, E. coli, Klebsiella pneumoniae, Serratia marcescens
TOXICITY: 1st generation cephalosporin
MOA: B-lactam drug that inhibits cell wall synthesis but are less susceptible to penicillinases. Bacteriocidal.
USES: PEcK (gram positive cocci)–Proteus mirabilis, E. coli, Klebsiella pneumoniae. Cefazolin used prior to surgery to prevent S. aureus wound infections
TOXICITY: hypersensitivity reactions, autoimmune hemolytic anemia, disulfiram-like reaction (inhibits acetaldehyde dehydrogenase and causes hangover symptoms, severe flushing hypotension, tachycardia with alcohol). Exhibits cross reactivity with penicillins. Increases nephrotoxicity of aminoglycosides.
Cefaclor
2nd generation cephalosporin
MOA: B-lactam drug that inhibits cell wall synthesis but are less susceptible to penicillinases. Bacteriocidal.
USES: HEN PEcKS (gram positive cocci)–Haemophilus influenzae, Enterobacter aerogenes, Neisseria spp., Proteus mirabilis, E. coli, Klebsiella pneumoniae, Serratia marcescens
TOXICITY: 1st generation cephalosporin
MOA: B-lactam drug that inhibits cell wall synthesis but are less susceptible to penicillinases. Bacteriocidal.
USES: PEcK (gram positive cocci)–Proteus mirabilis, E. coli, Klebsiella pneumoniae. Cefazolin used prior to surgery to prevent S. aureus wound infections
TOXICITY: hypersensitivity reactions, autoimmune hemolytic anemia, disulfiram-like reaction (inhibits acetaldehyde dehydrogenase and causes hangover symptoms, severe flushing hypotension, tachycardia with alcohol). Exhibits cross reactivity with penicillins. Increases nephrotoxicity of aminoglycosides.
Cefuroxime
2nd generation cephalosporin
MOA: B-lactam drug that inhibits cell wall synthesis but are less susceptible to penicillinases. Bacteriocidal.
USES: HEN PEcKS (gram positive cocci)–Haemophilus influenzae, Enterobacter aerogenes, Neisseria spp., Proteus mirabilis, E. coli, Klebsiella pneumoniae, Serratia marcescens
TOXICITY: 1st generation cephalosporin
MOA: B-lactam drug that inhibits cell wall synthesis but are less susceptible to penicillinases. Bacteriocidal.
USES: PEcK (gram positive cocci)–Proteus mirabilis, E. coli, Klebsiella pneumoniae. Cefazolin used prior to surgery to prevent S. aureus wound infections
TOXICITY: hypersensitivity reactions, autoimmune hemolytic anemia, disulfiram-like reaction (inhibits acetaldehyde dehydrogenase and causes hangover symptoms, severe flushing hypotension, tachycardia with alcohol). Exhibits cross reactivity with penicillins. Increases nephrotoxicity of aminoglycosides.
Ceftriaxone
3rd generation cephalosporin
MOA: B-lactam drug that inhibits cell wall synthesis but are less susceptible to penicillinases. Bactericidal.
USES:
TOXICITY: 1st generation cephalosporin
MOA: B-lactam drug that inhibits cell wall synthesis but are less susceptible to penicillinases. Bacteriocidal.
USES: PEcK (gram positive cocci)–Proteus mirabilis, E. coli, Klebsiella pneumoniae. Cefazolin used prior to surgery to prevent S. aureus wound infections
TOXICITY: hypersensitivity reactions, autoimmune hemolytic anemia, disulfiram-like reaction (inhibits acetaldehyde dehydrogenase and causes hangover symptoms, severe flushing hypotension, tachycardia with alcohol). Exhibits cross reactivity with penicillins. Increases nephrotoxicity of aminoglycosides.
Cefotaxime
3rd generation cephalosporin
MOA: B-lactam drug that inhibits cell wall synthesis but are less susceptible to penicillinases. Bactericidal.
USES: serious gram negative infections resistant to other B-lactams
TOXICITY: 1st generation cephalosporin
MOA: B-lactam drug that inhibits cell wall synthesis but are less susceptible to penicillinases. Bacteriocidal.
USES: PEcK (gram positive cocci)–Proteus mirabilis, E. coli, Klebsiella pneumoniae. Cefazolin used prior to surgery to prevent S. aureus wound infections
TOXICITY: hypersensitivity reactions, autoimmune hemolytic anemia, disulfiram-like reaction (inhibits acetaldehyde dehydrogenase and causes hangover symptoms, severe flushing hypotension, tachycardia with alcohol). Exhibits cross reactivity with penicillins. Increases nephrotoxicity of aminoglycosides.
Ceftazidime
3rd generation cephalosporin
MOA: B-lactam drug that inhibits cell wall synthesis but are less susceptible to penicillinases. Bactericidal.
USES: serious gram negative infections resistant to other B-lactams–Pseudomonas
TOXICITY: 1st generation cephalosporin
MOA: B-lactam drug that inhibits cell wall synthesis but are less susceptible to penicillinases. Bacteriocidal.
USES: PEcK (gram positive cocci)–Proteus mirabilis, E. coli, Klebsiella pneumoniae. Cefazolin used prior to surgery to prevent S. aureus wound infections
TOXICITY: hypersensitivity reactions, autoimmune hemolytic anemia, disulfiram-like reaction (inhibits acetaldehyde dehydrogenase and causes hangover symptoms, severe flushing hypotension, tachycardia with alcohol). Exhibits cross reactivity with penicillins. Increases nephrotoxicity of aminoglycosides.
Cefepime
4th generation cephalosporin
MOA: B-lactam drug that inhibits cell wall synthesis but are less susceptible to penicillinases. Bactericidal.
USES:
TOXICITY: 1st generation cephalosporin
MOA: B-lactam drug that inhibits cell wall synthesis but are less susceptible to penicillinases. Bacteriocidal.
USES: PEcK (gram positive cocci)–Proteus mirabilis, E. coli, Klebsiella pneumoniae. Cefazolin used prior to surgery to prevent S. aureus wound infections
TOXICITY: hypersensitivity reactions, autoimmune hemolytic anemia, disulfiram-like reaction (inhibits acetaldehyde dehydrogenase and causes hangover symptoms, severe flushing hypotension, tachycardia with alcohol). Exhibits cross reactivity with penicillins. Increases nephrotoxicity of aminoglycosides.
Ceftaroline
5th generation cephalosporin
MOA: B-lactam drug that inhibits cell wall synthesis but are less susceptible to penicillinases. Bactericidal.
USES: broad gram positive and gram negative organism coverage, including MRSA; does not cover pseudomonas.
TOXICITY: 1st generation cephalosporin
MOA: B-lactam drug that inhibits cell wall synthesis but are less susceptible to penicillinases. Bacteriocidal.
USES: PEcK (gram positive cocci)–Proteus mirabilis, E. coli, Klebsiella pneumoniae. Cefazolin used prior to surgery to prevent S. aureus wound infections
TOXICITY: hypersensitivity reactions, autoimmune hemolytic anemia, disulfiram-like reaction (inhibits acetaldehyde dehydrogenase and causes hangover symptoms, severe flushing hypotension, tachycardia with alcohol). Exhibits cross reactivity with penicillins. Increases nephrotoxicity of aminoglycosides.
Aztreonam
MOA: a monobactam; resistant to B-lactamase. Prevents peptidoglycan cross-linking by binding to penicillin-binding protein 3. Synergistic with aminoglycosides. No cross-allergenicity with penicillins.
USES: gram negative rods only–no activity against gram positive or anaerobes. For penicillin-allergic patients and those with renal insufficiency who cannot tolerate aminoglycosides.
TOXICITY: usually nontoxic. Occasional GI upset.
Meropenem
Cabapenem
MOA: B-lactamase-resistant capbapenem. Inhibit cell wall synthesis. Always administered with cilastatin (inhibitor of renal dehydropeptidase I) to decrease inactivation of drug in renal tubules.
USES: gram positive cocci, gram negative rods, and anaerobes. Wide spectrum, but significant side effects limit use to life threatening infections or after other drugs have failed.
TOXICITY: GI distress, skin rash, and CNS toxicity (seizures) at high plasma levels. **meropenem has a decreased risk of seizures and is stable to dehydropeptidase I
Ertapenem
Newer Cabapenem
MOA: broad-spectrum, B-lactamase-resistant capbapenem. Inhibit cell wall synthesis. Always administered with cilastatin (inhibitor of renal dehydropeptidase I) to decreased inactivation of drug in renal tubules.
USES: gram positive cocci, gram negative rods, and anaerobes. Wide spectrum, but significant side effects limit use to life threatening infections or after other drugs have failed. Limited pseudomonas coverage.
TOXICITY: GI distress, skin rash, and CNS toxicity (seizures) at high plasma levels.
Doripenem
Newer Cabapenem
MOA: broad-spectrum, B-lactamase-resistant capbapenem. Inhibit cell wall synthesis. Always administered with cilastatin (inhibitor of renal dehydropeptidase I) to decreased inactivation of drug in renal tubules.
USES: gram positive cocci, gram negative rods, and anaerobes. Wide spectrum, but significant side effects limit use to life threatening infections or after other drugs have failed. Limited pseudomonas coverage.
TOXICITY: GI distress, skin rash, and CNS toxicity (seizures) at high plasma levels.
Gentamicin
Aminoglycoside–30S inhibitor
MOA: bactericidal; inhibits formation of inititation complex and causes misreading of mRNA. Also blocks translocation. Requires O2 for uptake; therefore ineffective against anaerobes.
USES: severe, gram negative rod infections. Synergistic with B lactam antibiotics.
TOXICITY: nephrotoxicity, neuromuscular blockade, ototoxicity (especially when used with loop diuretics), teratogenic.
RESISTANCE: bacterial transferase enzymes inactivate the drug by acetylation, phosphorylation, or adenylation.
Neomycin
Aminoglycoside–30S inhibitor
MOA: bactericidal; inhibits formation of inititation complex and causes misreading of mRNA. Also blocks translocation. Requires O2 for uptake; therefore ineffective against anaerobes.
USES: severe, gram negative rod infections. Synergistic with B lactam antibiotics. Neomycin for bowel surgery.
TOXICITY: nephrotoxicity, neuromuscular blockade, ototoxicity (especially when used with loop diuretics), teratogenic.
RESISTANCE: bacterial transferase enzymes inactivate the drug by acetylation, phosphorylation, or adenylation.
Amikacin
Aminoglycoside–30S inhibitor
MOA: bactericidal; inhibits formation of inititation complex and causes misreading of mRNA. Also blocks translocation. Requires O2 for uptake; therefore ineffective against anaerobes.
USES: severe, gram negative rod infections. Synergistic with B lactam antibiotics.
TOXICITY: nephrotoxicity, neuromuscular blockade, ototoxicity (especially when used with loop diuretics), teratogenic.
RESISTANCE: bacterial transferase enzymes inactivate the drug by acetylation, phosphorylation, or adenylation.
Streptomycin
Aminoglycoside–30S inhibitor
MOA: bactericidal; inhibits formation of inititation complex and causes misreading of mRNA. Also blocks translocation. Requires O2 for uptake; therefore ineffective against anaerobes.
USES: severe, gram negative rod infections. Synergistic with B lactam antibiotics.
TOXICITY: nephrotoxicity, neuromuscular blockade, ototoxicity (especially when used with loop diuretics), teratogenic.
RESISTANCE: bacterial transferase enzymes inactivate the drug by acetylation, phosphorylation, or adenylation.
Tetracycline
MOA: bacteriostatic; binds 30s and prevents attachment of aminoacyl-tRNA; limited CNS penetration. Do not take with milk (calcium), antacids (calcium or magnesium), or iron-containing preparations because divalent cations inhibit absorption in gut.
USES: Borrelia burgdorferi, M pneumoniae. Drug’s ability to accumulate intracellularly makes it very effective against Rickettsia and Chlamydia. Also used to treat acne.
TOXICITY: GI distress, discoloration of Teeth and inhibition of bone growth in children, photosensitivity. Contraindicated in pregnancy.
RESISTANCE: decreased uptake or increased efflux out of bacterial cells by plasmid-encoded transport pumps.
Minocycline
MOA: bacteriostatic; binds 30s and prevents attachment of aminoacyl-tRNA; limited CNS penetration. Do not take with milk (calcium), antacids (calcium or magnesium), or iron-containing preparations because divalent cations inhibit absorption in gut.
USES: Borrelia burgdorferi, M pneumoniae. Drug’s ability to accumulate intracellularly makes it very effective against Rickettsia and Chlamydia. Also used to treat acne.
TOXICITY: GI distress, discoloration of Teeth and inhibition of bone growth in children, photosensitivity. Contraindicated in pregnancy.
RESISTANCE: decreased uptake or increased efflux out of bacterial cells by plasmid-encoded transport pumps.
Azithromycin
Macrolide
MOA: binds 50S subunit and inhibits translocation. Bacteriostatic.
Uses: atypical pneumonias-mycoplasma, chlamydia, legionella, STDs (chlamydia), gram positive cocci (strep if allergic to penicillin)
TOXICITY: GI motility issues, arrhythmia caused by prolonged QT, Canute cholestatic hepatitis, rash, eosinophilia. Increases serum concentration of theophyllines, oral anticoagulants.
RESISTANCE: methylation of 23s rRNA-binding site prevents binding of drug.
Clarithromycin
Macrolide
MOA: binds 50S subunit and inhibits translocation. Bacteriostatic.
Uses: atypical pneumonias-mycoplasma, chlamydia, legionella, STDs (chlamydia), gram positive cocci (strep if allergic to penicillin)
TOXICITY: GI motility issues, arrhythmia caused by prolonged QT, Canute cholestatic hepatitis, rash, eosinophilia. Increases serum concentration of theophyllines, oral anticoagulants.
RESISTANCE: methylation of 23s rRNA-binding site prevents binding of drug.
Chloramphenicol
MOA: blocks peptidyltransferase at 50s ribosomal subunit. Bacteriostatic.
USES: meningitis (Haemophilus influenzae, Neisseria meningitidis, Streptococcus pneumoniae) and Rocky Mountain Spotted Fever (Rickettsia rickettsii)
TOXICITY: anemia (dose dependent), aplastic anemia (dose independent), gray baby syndrome (in premature infants because they lack liver UDP-glucuronyl transferase)
RESISTANCE: plasmid-encoded acetyltransferase inactivates the drug.
Sulfisoxazole
Sulfonamide
MOA: inhibits folate synthesis. Para-aminobenzoic acid (PABA) antimetabolites inhibit dihydropteroate synthase. Bacteriostatic.
Uses: gram positive, gram negative, Nocardia, Chlamydia. Triple sulfas or SMX for simple UTI.
TOXICITY: hypersensitivity reactions, hemolysis if G6PD deficient, nephrotoxicity (Tubulointerstitial nephritis), photosensitivity, kernicterus in infants, displace other drugs from albumin (e.g. Warfarin)
RESISTANCE: altered enzyme (bacterial dihydropteroate synthase), decreased uptake, or increased PABA synthesis
Sulfadiazine
Sulfonamide
MOA: inhibits folate synthesis. Para-aminobenzoic acid (PABA) antimetabolites inhibit dihydropteroate synthase. Bacteriostatic.
Uses: gram positive, gram negative, Nocardia, Chlamydia. Triple sulfas or SMX for simple UTI.
TOXICITY: hypersensitivity reactions, hemolysis if G6PD deficient, nephrotoxicity (Tubulointerstitial nephritis), photosensitivity, kernicterus in infants, displace other drugs from albumin (e.g. Warfarin)
RESISTANCE: altered enzyme (bacterial dihydropteroate synthase), decreased uptake, or increased PABA synthesis
Norfloxacin
fluoroquinolone
MOA: inhibits DNA gyrate (topoisomerase II) and topoisomerase IV. bactericidal. Must not be taken with antacids.
Uses: gram negative rods of urinary and GI tracts, Neisseria, some gram positive organisms
TOXICITY: GI upset, super infections, skin rashes, headache, dizziness. Less commonly, can cause tendonitis, tendon rupture, leg cramps, and myalgias. Contraindicated in pregnancy, nursing mothers, and children under 18 due to possible damage to cartilage. Some may cause prolonged QT interval. May cause tendon rupture in people over 60y and in patients taking prednisone.
RESISTANCE: chromosome-encoded mutation in DNA gyrase, plasmid-mediated resistance, efflux pumps.
Levofloxacin
fluoroquinolone
MOA: inhibits DNA gyrate (topoisomerase II) and topoisomerase IV. bactericidal. Must not be taken with antacids.
Uses: gram negative rods of urinary and GI tracts, Neisseria, some gram positive organisms
TOXICITY: GI upset, super infections, skin rashes, headache, dizziness. Less commonly, can cause tendonitis, tendon rupture, leg cramps, and myalgias. Contraindicated in pregnancy, nursing mothers, and children under 18 due to possible damage to cartilage. Some may cause prolonged QT interval. May cause tendon rupture in people over 60y and in patients taking prednisone.
RESISTANCE: chromosome-encoded mutation in DNA gyrase, plasmid-mediated resistance, efflux pumps.
Ofloxacin
fluoroquinolone
MOA: inhibits DNA gyrate (topoisomerase II) and topoisomerase IV. bactericidal. Must not be taken with antacids.
Uses: gram negative rods of urinary and GI tracts, Neisseria, some gram positive organisms
TOXICITY: GI upset, super infections, skin rashes, headache, dizziness. Less commonly, can cause tendonitis, tendon rupture, leg cramps, and myalgias. Contraindicated in pregnancy, nursing mothers, and children under 18 due to possible damage to cartilage. Some may cause prolonged QT interval. May cause tendon rupture in people over 60y and in patients taking prednisone.
RESISTANCE: chromosome-encoded mutation in DNA gyrase, plasmid-mediated resistance, efflux pumps.
Sparfloxacin
fluoroquinolone
MOA: inhibits DNA gyrate (topoisomerase II) and topoisomerase IV. bactericidal. Must not be taken with antacids.
Uses: gram negative rods of urinary and GI tracts, Neisseria, some gram positive organisms
TOXICITY: GI upset, super infections, skin rashes, headache, dizziness. Less commonly, can cause tendonitis, tendon rupture, leg cramps, and myalgias. Contraindicated in pregnancy, nursing mothers, and children under 18 due to possible damage to cartilage. Some may cause prolonged QT interval. May cause tendon rupture in people over 60y and in patients taking prednisone.
RESISTANCE: chromosome-encoded mutation in DNA gyrase, plasmid-mediated resistance, efflux pumps.
Moxifloxacin
fluoroquinolone
MOA: inhibits DNA gyrate (topoisomerase II) and topoisomerase IV. bactericidal. Must not be taken with antacids.
Uses: gram negative rods of urinary and GI tracts, Neisseria, some gram positive organisms
TOXICITY: GI upset, super infections, skin rashes, headache, dizziness. Less commonly, can cause tendonitis, tendon rupture, leg cramps, and myalgias. Contraindicated in pregnancy, nursing mothers, and children under 18 due to possible damage to cartilage. Some may cause prolonged QT interval. May cause tendon rupture in people over 60y and in patients taking prednisone.
RESISTANCE: chromosome-encoded mutation in DNA gyrase, plasmid-mediated resistance, efflux pumps.
Gemifloxacin
fluoroquinolone
MOA: inhibits DNA gyrate (topoisomerase II) and topoisomerase IV. bactericidal. Must not be taken with antacids.
Uses: gram negative rods of urinary and GI tracts, Neisseria, some gram positive organisms
TOXICITY: GI upset, super infections, skin rashes, headache, dizziness. Less commonly, can cause tendonitis, tendon rupture, leg cramps, and myalgias. Contraindicated in pregnancy, nursing mothers, and children under 18 due to possible damage to cartilage. Some may cause prolonged QT interval. May cause tendon rupture in people over 60y and in patients taking prednisone.
RESISTANCE: chromosome-encoded mutation in DNA gyrase, plasmid-mediated resistance, efflux pumps.
Enoxacin
fluoroquinolone
MOA: inhibits DNA gyrate (topoisomerase II) and topoisomerase IV. bactericidal. Must not be taken with antacids.
Uses: gram negative rods of urinary and GI tracts, Neisseria, some gram positive organisms
TOXICITY: GI upset, super infections, skin rashes, headache, dizziness. Less commonly, can cause tendonitis, tendon rupture, leg cramps, and myalgias. Contraindicated in pregnancy, nursing mothers, and children under 18 due to possible damage to cartilage. Some may cause prolonged QT interval. May cause tendon rupture in people over 60y and in patients taking prednisone.
RESISTANCE: chromosome-encoded mutation in DNA gyrase, plasmid-mediated resistance, efflux pumps.
Nalidixic acid
Quinolone
MOA: inhibits DNA gyrate (topoisomerase II) and topoisomerase IV. bactericidal. Must not be taken with antacids.
Uses: gram negative rods of urinary and GI tracts, Neisseria, some gram positive organisms
TOXICITY: GI upset, super infections, skin rashes, headache, dizziness. Less commonly, can cause tendonitis, tendon rupture, leg cramps, and myalgias. Contraindicated in pregnancy, nursing mothers, and children under 18 due to possible damage to cartilage. Some may cause prolonged QT interval. May cause tendon rupture in people over 60y and in patients taking prednisone.
RESISTANCE: chromosome-encoded mutation in DNA gyrase, plasmid-mediated resistance, efflux pumps.
Isoniazid
Antimycobacterial prophylaxis against M. Tuberculosis
MOA: decreases synthesis of mycolic acids. Bacterial catalase-peroxidase (encoded by KatG) needed to convert INH to active metabolites
USES: Mycobacterium tuberculosis. The only agent used as solo prophylaxis against TB.
TOXICITY: neurotoxicity (usually presents as peripheral neuropathy),hepatotoxicity. Pyridoxine (vitamin B6) can prevent neurotoxicity (INH competes with B6 in synthesis of neurotransmitters and increases its urinary excretion leading to B6 deficiency)
**INH is metabolized by acetylation in the liver. Different half-lives in fast vs. slow acetylators–bimodal curve of drug concentration show pharmacological polymorphism in drug metabolism.
Rifampin
MOA: inhibits DNA-dependent RNA polymerase
USES: part of multi-agent drug therapy for Mycobacterium tuberculosis; delays resistance to dapsone when used for leprosy. Used for meningococcal prophylaxis and chemoprophylaxis in contacts of children with Haemophilus Influenzae type B.
TOXICITY: minor hepatotoxicity and drug interactions (increases P-450); orange body fluids. Rifabutin favored over rifampin in patients with HIV infection due to less cytochrome P-450 stimulation.
MECHANISM OF RESISTANCE: mutations reduce drug binding to RNA polymerase. Monotherapy rapidly leads to resistance.
Rifabutin
MOA: inhibits DNA-dependent RNA polymerase
USES: part of multi-agent drug therapy for Mycobacterium tuberculosis; delays resistance to dapsone when used for leprosy. Used for meningococcal prophylaxis and chemoprophylaxis in contacts of children with Haemophilus Influenzae type B.
TOXICITY: minor hepatotoxicity and drug interactions (increases P-450); orange body fluids. Rifabutin favored over rifampin in patients with HIV infection due to less cytochrome P-450 stimulation.
Pyrazinamide
MOA: uncertain. Thought to acidify intracellular environment via conversion to pyrazinoic acid. Effective in acidic pH of phagolysosomes, where TB engulfed by macrophages is found.
USES: P one RIPE therapy for Mycobacterium tuberculosis
TOXICITY: hyperuricemia, hepatotoxicity
Ethambutol
MOA: decreases carbohydrate polymerization of mycobacterium cell wall by blocking arabinosyltransferase
USES: Mycobacterium tuberculosis
TOXICITY: optic neuropathy (red-green color blindness)
Prophylaxis-endocarditis with surgical or dental procedures
Penicillins
Prophylaxis-Gonorrhea
Ceftriaxone
Prophylaxis-history of recurrent UTI
TMP-SMX
Prophylaxis-meningococcal infections
Ciprofloxacin (DOC), rifampin for children
Prophylaxis-pregnancy women carrying group B strep
Ampicillin
Prophylaxis-prevention of gonococcal or chlamydial conjunctivitis in newborn
Erythromycin ointment
Prophylaxis-prevention of post surgical infection due to S. Aureus
Cefazolin
Prophylaxis-strep pharyngitis in child with prior rheumatic fever
Oral penicillin
Prophylaxis-syphillis
Benzathine penicillin G
Prophylaxis in HIV-Pneumocystis pneumonia
CD4<200 TMP-SMX
Prophylaxis in HIV-pneumocystis pneumonia and toxoplasmosis
CD4<100 TMP-SMX
Prophylaxis HIV-Mycobacterium avium complex
CD4<50 Azithromycin
Amphotericin B
Anti-fungal
MOA: binds ergosterol and forms membrane pores that allow leakage of electrolytes
USES: serious systemic mycoses, not for non-invasive infections. Cryptococcus, Blastomyces, Coccidioides, Histoplasma, Candida, Mucor. Intrathecally for fungal meningitis. Supplement K+ and Mg++ because of altered renal tubule permeability.
TOXICITY: fever/chills, hypotension, nephrotoxicity (causes both decreased GFR and divert toxic effects on tubular epithelium), arrhythmias, anemia, IV phlebitis. Hydration decreases nephrotoxicity. Liposomal Amphotericin decreases toxicity.
Nystatin
MOA: same as Amphotericin B (binds ergosterol and forms pores in membranes). Topical form because too toxic for systemic use.
USES: only mucocutaneous infections, not systemic. “Swish and swallow” for oral candidiasis; topical for diaper rash or vaginal candidiasis.
Fluconazole
MOA: inhibits fungal (ergosterol) synthesis, by inhibiting the P-450 enzyme that converts lanosterol to
USES: local and less serious systemic mycoses; chronic suppression of cryptococcal meningitis in AIDS patients and Candida infections of all types. Itraconazole for Blastomyces, Coccidioides, Histoplasma. Clotrimazole and miconazole for topical fungal infections.
TOXICITY: testosterone synthesis inhibition (gynecomastia), liver dysfunction (inhibits cytochrome P-450), increases levels of P450 metabolized drugs (cyclosporine, warfarin)
Ketoconazole
MOA: inhibits fungal (ergosterol) synthesis, by inhibiting the P-450 enzyme that converts lanosterol to
USES: local and less serious systemic mycoses; chronic suppression of cryptococcal meningitis in AIDS patients and Candida infections of all types. Itraconazole for Blastomyces, Coccidioides, Histoplasma. Clotrimazole and miconazole for topical fungal infections.
TOXICITY: testosterone synthesis inhibition (gynecomastia), liver dysfunction (inhibits cytochrome P-450), increases levels of P450 metabolized drugs (cyclosporine, warfarin)
Clotrimazole
MOA: inhibits fungal (ergosterol) synthesis, by inhibiting the P-450 enzyme that converts lanosterol to
USES: local and less serious systemic mycoses; chronic suppression of cryptococcal meningitis in AIDS patients and Candida infections of all types. Itraconazole for Blastomyces, Coccidioides, Histoplasma. Clotrimazole and miconazole for topical fungal infections.
TOXICITY: testosterone synthesis inhibition (gynecomastia), liver dysfunction (inhibits cytochrome P-450), increases levels of P450 metabolized drugs (cyclosporine, warfarin)
Miconazole
MOA: inhibits fungal (ergosterol) synthesis, by inhibiting the P-450 enzyme that converts lanosterol to
USES: local and less serious systemic mycoses; chronic suppression of cryptococcal meningitis in AIDS patients and Candida infections of all types. Itraconazole for Blastomyces, Coccidioides, Histoplasma. Clotrimazole and miconazole for topical fungal infections.
TOXICITY: testosterone synthesis inhibition (gynecomastia), liver dysfunction (inhibits cytochrome P-450), increases levels of P450 metabolized drugs (cyclosporine, warfarin)
Itraconazole
MOA: inhibits fungal (ergosterol) synthesis, by inhibiting the P-450 enzyme that converts lanosterol to
USES: local and less serious systemic mycoses; chronic suppression of cryptococcal meningitis in AIDS patients and Candida infections of all types. Itraconazole for Blastomyces, Coccidioides, Histoplasma. Clotrimazole and miconazole for topical fungal infections.
TOXICITY: testosterone synthesis inhibition (gynecomastia), liver dysfunction (inhibits cytochrome P-450), increases levels of P450 metabolized drugs (cyclosporine, warfarin)
Voriconazole
MOA: inhibits fungal (ergosterol) synthesis, by inhibiting the P-450 enzyme that converts lanosterol to
USES: local and less serious systemic mycoses; chronic suppression of cryptococcal meningitis in AIDS patients and Candida infections of all types. Itraconazole for Blastomyces, Coccidioides, Histoplasma. Clotrimazole and miconazole for topical fungal infections.
TOXICITY: testosterone synthesis inhibition (gynecomastia), liver dysfunction (inhibits cytochrome P-450), increases levels of P450 metabolized drugs (cyclosporine, warfarin)
Flucytosine
MOA: inhibits DNA and RNA biosynthesis by conversion to 5-fluorouracil by cytosine deaminase–blocks thymidylate synthetase
USES: systemic fungal infections (especially meningitis caused by cryptococcus) in combination with Amphotericin B
TOXICITY: bone marrow suppression
Caspofungin
MOA: inhibits cell wall synthesis by inhibiting synthesis of B-glucan
USES: invasive aspergillosis, candida.
TOXICITY: GI upset, flushing (by histamine release)
Micafungin
MOA: inhibits cell wall synthesis by inhibiting synthesis of B-glucan
USES: invasive aspergillosis, candida.
TOXICITY: GI upset, flushing (by histamine release)
Anidulafungin
MOA: inhibits cell wall synthesis by inhibiting synthesis of B-glucan
USES: invasive aspergillosis, candida.
TOXICITY: GI upset, flushing (by histamine release)
Terbinafine
MOA: inhibits the fungal enzyme squalene epoxidase (ergosterol biosynthesis inhibitor)
USES: used to treat dermatophytoses–especially onychomycosis (fungal infection in finger or toe nails)
TOXICITY: GI upset, headaches, hepatotoxicity, taste disturbance
Griseofulvin
MOA: interferes with microtubule function; disrupts mitosis. Deposits in keratin-containing tissues (e.g. Nails)
USES: oral treatment of superficial infections–inhibits growth of dermatophytes (tinea, ringworm)
TOXICITY: teratogenic, carcinogenic, confusion, headaches, increases P450 and warfarin metabolism.
Chloroquine
MOA: blocks detoxification of heme into hemozoin. Heme accumulates and is toxic to plasmodia.
USES: plasmodial erythrocyte infection (not liver). treatment of plasmodial species other than P. Falciparum (frequency of resistance to falciparum is too great). Resistance due to membrane pump that decreases intracellular concentration of drug. Treat P. Falciparum with artemether/lumafantrine or atovoquone/proguanil. For life-threatening malaria, use quinidine in US or artesunate.
TOXICITY: retinopathy, pruritis
Artemether/lumefantrine
MOA: not known; drug combo artemisinin derivative and lumafantrine
USES: acute, uncomplicated p. Falciparum; treat chloroquine-resistant strains; NOT prophylaxis or severe
Mebendazole
Anti-helminthic
MOA: binds worm tubulin and interferes with organellar transport–immobilizes helminth.
USES: enterobiasis (pinworm), trichuriasis (whip worm), ascariasis
Praziquantel
Antihelminthic therapy
MOA: increases cellular calcium–>permeability leads to death of organism
USES: all species of schistosoma, infection due to liver flukes
Zanamivir
MOA: inhibits viral neuraminidase–prevents new viral particles from being released
USES: treatment and prevention of both influenza A and B
Oseltamivir
MOA: inhibits viral neuraminidase–prevents new viral particles from being released
USES: treatment and prevention of both influenza A and B
Acyclovir
MOA: monophosphorylated by HSV/VZV thymidine kinase and not phosphorylated in uninfected cells, so few adverse effects. Guanosine analog. Triphosphate formed by cellular enzymes. Preferentially inhibits viral DNA polymerase by chain termination.
USES: HSV and VZV. Weak activity against EBV. No activity against CMV. Used for HSV-induced mucocutaneous and genital lesions as well as encephalitis. Prophylaxis in immunocompromised patients. No effect on latent forms of HSV and VZV. Valacyclovir, a prodrug of acyclovir, has better oral bioavailability.
TOXICITY: obstructive crystalline nephropathy and acute renal failure if not adequately hydrated. When the concentration in collecting duct exceeds it’s solubility.
RESISTANCE: mutated viral thymidine kinase,
Famciclovir
MOA: monophosphorylated by HSV/VZV thymidine kinase and not phosphorylated in uninfected cells, so few adverse effects. Guanosine analog. Triphosphate formed by cellular enzymes. Preferentially inhibits viral DNA polymerase by chain termination.
USES: HSV and VZV. Weak activity against EBV. No activity against CMV. Used for HSV-induced mucocutaneous and genital lesions as well as encephalitis. Prophylaxis in immunocompromised patients. No effect on latent forms of HSV and VZV. Valacyclovir, a prodrug of acyclovir, has better oral bioavailability.
TOXICITY: obstructive crystalline nephropathy and acute renal failure if not adequately hydrated. When the concentration in collecting duct exceeds it’s solubility.
RESISTANCE: mutated viral thymidine kinase,
Valacyclovir
MOA: monophosphorylated by HSV/VZV thymidine kinase and not phosphorylated in uninfected cells, so few adverse effects. Guanosine analog. Triphosphate formed by cellular enzymes. Preferentially inhibits viral DNA polymerase by chain termination.
USES: HSV and VZV. Weak activity against EBV. No activity against CMV. Used for HSV-induced mucocutaneous and genital lesions as well as encephalitis. Prophylaxis in immunocompromised patients. No effect on latent forms of HSV and VZV. Valacyclovir, a prodrug of acyclovir, has better oral bioavailability.
TOXICITY: obstructive crystalline nephropathy and acute renal failure if not adequately hydrated. When the concentration in collecting duct exceeds it’s solubility.
RESISTANCE: mutated viral thymidine kinase,
Ganciclovir
MOA: synthetic analog of 2-deoxyguanine. Converted to ganciclovir mono phosphate by CMV during infection; subsequently, cellular kinases catalyze the formation of gancyclovir diphosphate and triphosphate–activated drug inhibits DNA polymerase and suppresses chain elongation.
USES: CMV, especially in immunocompromised patients. Valganciclovir, a prodrug of ganciclovir, has better oral bioavailability.
TOXICITY: leukopenia, neutropenia, thrombocytopenia, renal toxicity. More toxic to host enzymes than acyclovir.
RESISTANCE: mutated CMV DNA polymerase or lack of viral kinase.
Foscarnet
MOA: viral DNA polymerase inhibitor that binds to the pyrophosphate-binding site of the enzyme. Does not require activation by viral kinase.
USES: CMV retinitis in immunocompromised patients when ganciclovir fails; acyclovir-resistant HSVZ
TOXICITY: nephrotoxicity, electrolyte abnormalities can lead to seizures. Foscarnet is a pyrophosphate analog that can chelate calcium and cause magnesium wasting leading to decreased PTH which exacerbates hypocalcemia. (Remember dramatic decreases in magnesium inhibit PTH)
RESISTANCE: mutated DNA polymerase
Cidofovir
MOA: preferentially inhibits viral DNA polymerase. Does not require phosphorylation by viral kinase.
USES: CMV retinitis in immunocompromised patients; acyclovir-resistant HSV. Long half life.
TOXICITY: nephrotoxicity (co administer with probenecid and IV saline to decrease toxicity)
Ribavirin
MOA: inhibits synthesis of guanine nucleotides by competitively inhibiting inosine monophosphate dehydrogenase
USES: RSV! Chronic hepatitis C
TOXICITY: hemolytic anemia. Severe teratogen
Atazanavir
Protease inhibitor
MOA: assembly of virions depends on HIV-1 protease, which cleaves the polypeptide products of HIV mRNA into their functional parts. Thus, protease inhibitors prevent maturation of new viruses.
TOXICITY: hyperglycemia, GI intolerance, lipodystrophy, nephropathy, hematuria
Darunavir
Protease inhibitor
MOA: assembly of virions depends on HIV-1 protease, which cleaves the polypeptide products of HIV mRNA into their functional parts. Thus, protease inhibitors prevent maturation of new viruses.
TOXICITY: hyperglycemia, GI intolerance, lipodystrophy, nephropathy, hematuria
Fosamprenavir
Protease inhibitor
MOA: assembly of virions depends on HIV-1 protease, which cleaves the polypeptide products of HIV mRNA into their functional parts. Thus, protease inhibitors prevent maturation of new viruses.
TOXICITY: hyperglycemia, GI intolerance, lipodystrophy, nephropathy, hematuria
Indinavir
Protease inhibitor
MOA: assembly of virions depends on HIV-1 protease, which cleaves the polypeptide products of HIV mRNA into their functional parts. Thus, protease inhibitors prevent maturation of new viruses.
TOXICITY: hyperglycemia, GI intolerance, lipodystrophy, nephropathy, hematuria
Lopinavir
Protease inhibitor
MOA: assembly of virions depends on HIV-1 protease, which cleaves the polypeptide products of HIV mRNA into their functional parts. Thus, protease inhibitors prevent maturation of new viruses.
TOXICITY: hyperglycemia, GI intolerance, lipodystrophy, nephropathy, hematuria
Ritonavir
Protease inhibitor
MOA: assembly of virions depends on HIV-1 protease, which cleaves the polypeptide products of HIV mRNA into their functional parts. Thus, protease inhibitors prevent maturation of new viruses. Ritonavir can boost other drug concentrations by inhibiting p-450
TOXICITY: hyperglycemia, GI intolerance, lipodystrophy, nephropathy, hematuria. Inhibitor of CYP-450 so increases drug concentrations of those metabolized by CYP -450.
Saquinavir
Protease inhibitor
MOA: assembly of virions depends on HIV-1 protease, which cleaves the polypeptide products of HIV mRNA into their functional parts. Thus, protease inhibitors prevent maturation of new viruses.
TOXICITY: hyperglycemia, GI intolerance, lipodystrophy, nephropathy, hematuria
Abacavir
NRTI
MOA: competitively inhibit nucleotide binding to reverse transcriptase and terminate the DNA chain (lack a 3’ OH group). Nucleoside–needs to be phosphorylated to be active.
TOXICITY: bone marrow suppression (can be reversed with granulocyte-stimulating factor and erythropoietin), peripheral neuropathy, lactic acidosis, rash, anemia, pancreatitis
Didanosine
NRTI
MOA: competitively inhibit nucleotide binding to reverse transcriptase and terminate the DNA chain (lack a 3’ OH group). Nucleoside–needs to be phosphorylated to be active.
TOXICITY: bone marrow suppression (can be reversed with granulocyte-stimulating factor and erythropoietin), peripheral neuropathy, lactic acidosis, rash, anemia, pancreatitis
Emtricitabine
NRTI
MOA: competitively inhibit nucleotide binding to reverse transcriptase and terminate the DNA chain (lack a 3’ OH group). Nucleoside–needs to be phosphorylated to be active.
TOXICITY: bone marrow suppression (can be reversed with granulocyte-stimulating factor and erythropoietin), peripheral neuropathy, lactic acidosis, rash, anemia, pancreatitis
Lamivudine
NRTI
MOA: competitively inhibit nucleotide binding to reverse transcriptase and terminate the DNA chain (lack a 3’ OH group). Nucleoside–needs to be phosphorylated to be active.
TOXICITY: bone marrow suppression (can be reversed with granulocyte-stimulating factor and erythropoietin), peripheral neuropathy, lactic acidosis, rash, anemia, pancreatitis
Stavudine
NRTI
MOA: competitively inhibit nucleotide binding to reverse transcriptase and terminate the DNA chain (lack a 3’ OH group). Nucleoside–needs to be phosphorylated to be active.
TOXICITY: bone marrow suppression (can be reversed with granulocyte-stimulating factor and erythropoietin), peripheral neuropathy, lactic acidosis, rash, anemia, pancreatitis
Tenofovir
NRTI
MOA: competitively inhibit nucleotide binding to reverse transcriptase and terminate the DNA chain (lack a 3’ OH group). Nucleotide–does NOT need to be phosphorylated to be active.
TOXICITY: bone marrow suppression (can be reversed with granulocyte-stimulating factor and erythropoietin), peripheral neuropathy, lactic acidosis, rash, anemia, pancreatitis
Zidovudine
Formerly AZT
NRTI
MOA: competitively inhibit nucleotide binding to reverse transcriptase and terminate the DNA chain (lack a 3’ OH group). Nucleoside–needs to be phosphorylated to be active. Used for general prophylaxis and during pregnancy to decrease risk of transmission to fetus.
TOXICITY: bone marrow suppression (can be reversed with granulocyte-stimulating factor and erythropoietin), peripheral neuropathy, lactic acidosis, rash, anemia, pancreatitis
Efavirenz
NNRTI
MOA: bind to reverse transcriptase at site different from NRTIs. Do not require phosphorylation to be active or compete with nucleotides.
TOXICITY: rash and hepatotoxicity are common. Vivid dreams and CNS symptoms common with efavirenz. Contraindicated in pregnancy.
Nevirapine
NNRTI
MOA: bind to reverse transcriptase at site different from NRTIs. Do not require phosphorylation to be active or compete with nucleotides.
TOXICITY: rash and hepatotoxicity are common.
Delavirdine
NNRTI
MOA: bind to reverse transcriptase at site different from NRTIs. Do not require phosphorylation to be active or compete with nucleotides.
TOXICITY: rash and hepatotoxicity are common. Contraindicated in pregnancy.
Raltegravir
Integrase inhibitor
MOA: inhibits HIV genome integration into host cell chromosome by reversibly inhibiting HIV integrase
TOXICITY: hypercholesterolemia
Enfuvirtide
Fusion inhibitor
MOA: binds gp41 and inhibits viral entry
TOXICITY: skin reaction at injection site
Maraviroc
Fusion inhibitor
MOA: binds CCR-5 on surface of T cells/monocytes, inhibiting interaction with gp120
TOXICITY: skin reaction at injection site
Daptomycin
MOA: lipopeptide that disrupts cell membrane of gram positive cocci.
USES: S. Aureus skin infections, bacteremia, endocarditis, VRE
TOXICITY: myopathy, rhabdomyolysis
Metronidazole
MOA: forms toxic free radical metabolites on the bacterial cell that damage DNA. Bactericidal, antiprotozoal.
USES: treats Giardia, Entamoeba, Trichomonas, Gardnerella vaginalis, Anaerobes (Bacteroides, C. Difficile). Used with a proton pump and clarithromycin for triple therapy against h. Pylori.
TOXICITY: disulfiram-like reactions (severe flushing, tachycardia, hypotension) with alcohol, headache, metallic taste
Interferons
MOA: glycoproteins normally synthesized by virus-infected cells, exhibiting a wide range of antiviral and antitumoral properties
USES: IFN-a: chronic hepatitis B and C, Kaposi sarcoma, hairy cell leukemia, condyloma acuminatum, renal cell carcinoma, malignant melanoma. IFN-B: MS. IFN-gamma: chronic granulomatous disease.
TOXICITY: neutropenia, myopathy
Ribavirin
MOA: inhibits synthesis of guanine nucleotides by competitively inhibiting inosine monophosphate dehydrogenase. IMP cannot be converted to GMP.
USES: chronic HCV, also used in RSV (palivizumab preferred in children)
TOXICITY: hemolytic anemia, severe teratogen
Simeprevir
MOA: HCV protease inhibitor; prevents viral replication
USES: chronic HCV in combination with ribavirin and peginterferon Alfa.
TOXICITY: photosensitivity reactions, rash
Sofosbuvir
MOA: inhibits HCV RNA-dependent RNA polymerase acting as a chain terminator
USES: chronic HCV in combination with ribavirin, +/- peginterferon Alfa.
TOXICITY: fatigue, headache, nausea
Red man syndrome
Diffuse flushing following vancomycin treatment. Cn largely prevent by pretreatment with antihistamines and slow infusion rate
Prophylaxis for M. Tuberculosis
Isoniazid
Prophylaxis for M. Avium-intracellulare
Azithromycin, rifabutin
Palivizumab
Monoclonal antibody against F protein of paramyxoviruses. Prevents pneumonia caused by RSV infection in premature infants.
Fidaxomicin
Treatment for recurrent cases of C. Difficile. Inhibits sigma subunit of RNA polymerase. Oral drug with limited systemic absorption.
