Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

First Aid > Microbiology - Antimicrobials (1) > Flashcards

Microbiology - Antimicrobials (1) Flashcards

1
Q

Antimicrobial therapy (179)

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Penicillin G, V

  • Examples
  • Mechanism
  • Clinical use
  • Toxicity
  • Mechanism of resistance
A
  • Examples
    • Penicillin G (IV and IM form), penicillin V (oral).
    • Prototype β-lactam antibiotics.
  • Mechanism
    • Bind penicillin-binding proteins (transpeptidases).
    • Block transpeptidase cross-linking of peptidoglycan.
    • Activate autolytic enzymes.
  • Clinical use
    • Mostly used for gram-positive organisms (S. pneumoniae, 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.
  • Mechanism of resistance
    • Penicillinase in bacteria (a type of β-lactamase) cleaves β-lactam ring.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Ampicillin, amoxicillin (aminopenicillins, penicillinase-sensitive penicillins)

  • Mechanism
  • Clinical use
  • Toxicity
  • Mechanism of resistance
A
  • Mechanism
    • Same as penicillin.
      • Bind penicillin-binding proteins (transpeptidases).
      • Block transpeptidase cross-linking of peptidoglycan.
      • Activate autolytic enzymes.
    • Wider spectrum
    • Penicillinase sensitive.
    • Also combine with clavulanic acid to protect against β-lactamase.
    • AMinoPenicillins are AMPed-up penicillin.
    • AmOxicillin has greater Oral bioavailability than ampicillin.
  • Clinical use
    • Extended-spectrum penicillin—Haemophilus influenzae, E. coli, Listeria monocytogenes, Proteus mirabilis, Salmonella, Shigella, enterococci.
    • Coverage: ampicillin/amoxicillin HELPSS kill enterococci.
  • Toxicity
    • Hypersensitivity reactions; rash; pseudomembranous colitis.
  • Mechanism of resistance
    • Penicillinase in bacteria (a type of β-lactamase) cleaves β-lactam ring.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Oxacillin, nafcillin, dicloxacillin (penicillinase-resistant penicillins)

  • Mechanism
  • Clinical use
  • Toxicity
A
  • Mechanism
    • Same as penicillin.
      • Bind penicillin-binding proteins (transpeptidases).
      • Block transpeptidase cross-linking of peptidoglycan.
      • Activate autolytic enzymes.
    • Narrow spectrum
    • Penicillinase resistant because bulky R group blocks access of β-lactamase to β-lactam ring.
  • Clinical use
    • S. aureus (except MRSA; resistant because of altered penicillin-binding protein target site).
    • “Use naf (nafcillin) for staph.”
  • Toxicity
    • Hypersensitivity reactions, interstitial nephritis.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Ticarcillin, piperacillin (antipseudomonals)

  • Mechanism
  • Clinical use
  • Toxicity
A
  • Mechanism
    • Same as penicillin.
      • Bind penicillin-binding proteins (transpeptidases).
      • Block transpeptidase cross-linking of peptidoglycan.
      • Activate autolytic enzymes.
    • Extended spectrum.
  • Clinical use
    • Pseudomonas spp. and gram-negative rods
    • Susceptible to penicillinase
    • Use with β-lactamase inhibitors.
  • Toxicity
    • Hypersensitivity reactions.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

β-lactamase inhibitors

A
  • CAST
    • Clavulanic Acid
    • Sulbactam
    • Tazobactam
  • Often added to penicillin antibiotics to protect the antibiotic from destruction by β-lactamase (penicillinase).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Cephalosporins (generations I, II, III, IV, V)

  • Mechanism
  • Organisms typically not covered by cephalosporins
  • Clinical use
    • 1st generation
    • 2nd generation
    • 3rd generation
    • 4th generation
    • 5th generation
  • Toxicity
A
  • Mechanism
    • β-lactam drugs that inhibit cell wall synthesis but are less susceptible to penicillinases.
    • Bactericidal.
  • Organisms typically not covered by cephalosporins
    • LAME: Listeria, Atypicals (Chlamydia, Mycoplasma), MRSA, and Enterococci.
    • Exception: ceftaroline covers MRSA.
  • Clinical use
    • 1st generation (cefazolin, cephalexin)
      • Gram-positive cocci, Proteus mirabilis, E. coli, Klebsiella pneumoniae.
        • PEc_K_.
      • Cefazolin used prior to surgery to prevent S. aureus wound infections.
    • 2nd generation (cefoxitin, cefaclor, cefuroxime)
      • Gram-positive cocci, Haemophilus influenzae, Enterobacter aerogenes, Neisseria spp., Proteus mirabilis, E. coli, Klebsiella pneumoniae, Serratia marcescens.
        • HEN PEc_KS_.
    • 3rd generation (ceftriaxone, cefotaxime, ceftazidime)
      • Serious gram-negative infections resistant to other β-lactams.
      • Ceftriaxone—meningitis and gonorrhea.
      • Ceftazidime—Pseudomonas.
    • 4th generation (cefepime)
      • Increase activity against Pseudomonas and gram-positive organisms.
    • 5th generation (ceftaroline)
      • Broad gram-positive and gram-negative organism coverage, including MRSA
      • Does not cover Pseudomonas.
  • Toxicity
    • Hypersensitivity reactions, vitamin K deficiency.
    • Low cross-reactivity with penicillins.
    • Increased nephrotoxicity of aminoglycosides.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Aztreonam

  • Mechanism
  • Clinical use
  • Toxicity
A
  • Mechanism
    • A monobactam
    • Resistant to β-lactamases.
    • Prevents peptidoglycan cross-linking by binding to penicillin-binding protein 3.
    • Synergistic with aminoglycosides.
    • No cross-allergenicity with penicillins.
  • Clinical use
    • Gram-negative rods only—no activity against gram-positives or anaerobes.
    • For penicillin-allergic patients and those with renal insufficiency who cannot tolerate aminoglycosides.
  • Toxicity
    • Usually nontoxic; occasional GI upset.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Carbapenems

  • Examples
  • Mechanism
  • Clinical use
  • Toxicity
A
  • Examples
    • Imipenem, meropenem, ertapenem, doripenem.
  • Mechanism
    • Imipenem
      • A broad-spectrum, β-lactamase– resistant carbapenem.
      • Always administered with cilastatin (inhibitor of renal dehydropeptidase I) to decrease inactivation of drug in renal tubules.
      • With imipenem, “the kill is lastin’ with cilastatin.”
    • Newer carbapenems include ertapenem (limited Pseudomonas coverage) and doripenem.
  • Clinical use
    • 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.
    • Meropenem has a decreased risk of seizures and is stable to dehydropeptidase I.
  • Toxicity
    • GI distress, skin rash, and CNS toxicity (seizures) at high plasma levels.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Vancomycin

  • Mechanism
  • Clinical use
  • Toxicity
  • Mechanism of resistance
A
  • Mechanism
    • Inhibits cell wall peptidoglycan formation by binding D-ala D-ala portion of cell wall precursors.
    • Bactericidal.
  • Clinical use
    • 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 man syndrome (can largely prevent by pretreatment with antihistamines and slow infusion rate).
  • Mechanism of resistance
    • Occurs in bacteria via amino acid modification of D-ala D-ala to D-ala D-lac.
    • “Pay back 2 D-alas (dollars) for vandalizing (vancomycin).”
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Protein synthesis inhibitors

  • General
  • 30S inhibitors
  • 50S inhibitors
A
  • General
    • Specifically target smaller bacterial ribosome (70S, made of 30S and 50S subunits), leaving human ribosome (80S) unaffected.
    • “Buy AT 30, CCEL (sell) at 50.”
  • 30S inhibitors
    • A = Aminoglycosides [bactericidal]
    • T = Tetracyclines [bacteriostatic]
  • 50S inhibitors
    • C = Chloramphenicol, Clindamycin [bacteriostatic]
    • E = Erythromycin (macrolides) [bacteriostatic]
    • L = Linezolid [variable]
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Aminoglycosides

  • Examples
  • Mechanism
  • Clinical use
  • Toxicity
  • Mechanism of resistance
A
  • Examples
    • Gentamicin, Neomycin, Amikacin, Tobramycin, Streptomycin.
    • “Mean” (aminoglycoside) GNATS caNNOT** kill anaerobes.**
  • Mechanism
    • Bactericidal
    • Inhibit formation of initiation complex and cause misreading of mRNA.
      • Also block translocation.
    • Require O2 for uptake; therefore ineffective against anaerobes.
    • A “initiates” the Alphabet.
  • Clinical use
    • Severe gram-negative rod infections.
    • Synergistic with β-lactam antibiotics.
    • Neomycin for bowel surgery.
  • Toxicity
    • Nephrotoxicity (especially when used with cephalosporins)
    • Neuromuscular blockade
    • Ototoxicity (especially when used with loop diuretics)
    • Teratogen
    • “Mean” (aminoglycoside) GNATS caNNOT** kill anaerobes.**
  • Mechanism of resistance
    • Bacterial transferase enzymes inactivate the drug by acetylation, phosphorylation, or adenylation.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Tetracyclines

  • Examples
  • Mechanism
  • Clinical use
  • Toxicity
  • Mechanism of resistance
A
  • Examples
    • Tetracycline, doxycycline, minocycline.
  • Mechanism
    • Bacteriostatic
    • Bind to 30S and prevent 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 (Ca2+), antacids (Ca2+ or Mg2+), or iron-containing preparations because divalent cations inhibit its absorption in the gut.
  • Clinical use
    • 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.
  • Mechanism of resistance
    • Decreased uptake or increased efflux out of bacterial cells by plasmid-encoded transport pumps.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Macrolides

  • Examples
  • Mechanism
  • Clinical use
  • Toxicity
  • Mechanism of resistance
A
  • Examples
    • Azithromycin, clarithromycin, erythromycin.
  • Mechanism
    • Inhibit protein synthesis by blocking translocation (“macroslides”)
    • Bind to the 23S rRNA of the 50S ribosomal subunit.
    • Bacteriostatic.
  • Clinical use
    • Atypical pneumonias (Mycoplasma, Chlamydia, Legionella), STDs (for Chlamydia), and gram-positive cocci (streptococcal infections in patients allergic to penicillin).
  • Toxicity
    • MACRO: Gastrointestinal Motility issues, Arrhythmia caused by prolonged QT, acute Cholestatic hepatitis, Rash, eOsinophilia.
    • Increases serum concentration of theophyllines, oral anticoagulants.
  • Mechanism of resistance
    • Methylation of 23S rRNA-binding site prevents binding of drug.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Chloramphenicol

  • Mechanism
  • Clinical use
  • Toxicity
  • Mechanism of resistance
A
  • Mechanism
    • Blocks peptidyltransferase at 50S ribosomal subunit.
    • Bacteriostatic.
  • Clinical use
    • Meningitis (Haemophilus influenzae, Neisseria meningitidis, Streptococcus pneumoniae) and Rocky Mountain spotted fever (Rickettsia rickettsii).
    • Limited use owing to toxicities but often still used in developing countries because of low cost.
  • Toxicity
    • Anemia (dose dependent), aplastic anemia (dose independent), gray baby syndrome (in premature infants because they lack liver UDP-glucuronyl transferase).
  • Mechanism of resistance
    • Plasmid-encoded acetyltransferase inactivates the drug.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Clindamycin

  • Mechanism
  • Clinical use
  • Toxicity
A
  • Mechanism
    • Blocks peptide transfer (translocation) at 50S ribosomal subunit.
    • Bacteriostatic.
  • Clinical use
    • Anaerobic infections (e.g., Bacteroides spp., Clostridium perfringens) in aspiration pneumonia, lung abscesses, and oral infections.
    • Also effective against invasive Group A streptococcal (GAS) infection.
    • Treats anaerobes above the diaphragm vs. metronidazole (anaerobic infections below diaphragm).
  • Toxicity
    • Pseudomembranous colitis (C. difficile overgrowth), fever, diarrhea.
17
Q

Sulfonamides

  • Examples
  • Mechanism
  • Clinical use
  • Toxicity
  • Mechanism of resistance
A
  • Examples
    • Sulfamethoxazole (SMX), sulfisoxazole, sulfadiazine.
  • Mechanism
    • Inhibit folate synthesis.
    • Para-aminobenzoic acid (PABA) antimetabolites inhibit dihydropteroate synthase.
    • Bacteriostatic.
  • Clinical use
    • 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).
  • Mechanism of resistance
    • Altered enzyme (bacterial dihydropteroate synthase), decreased uptake, or increased PABA synthesis.
18
Q

Trimethoprim

  • Mechanism
  • Clinical use
  • Toxicity
A
  • Mechanism
    • Inhibits bacterial dihydrofolate reductase.
    • Bacteriostatic.
  • Clinical use
    • Used in combination with sulfonamides (trimethoprim-sulfamethoxazole [TMP-SMX]), causing sequential block of folate synthesis.
      • TMP: Treats Marrow Poorly.
    • Combination used for UTIs, Shigella, Salmonella, Pneumocystis jirovecii pneumonia treatment and prophylaxis, toxoplasmosis prophylaxis.
  • Toxicity
    • Megaloblastic anemia, leukopenia, granulocytopenia.
      • TMP: Treats Marrow Poorly
    • May alleviate with supplemental folinic acid.
19
Q

Fluoroquinolones

  • Examples
  • Mechanism
  • Clinical use
  • Toxicity
  • Mechanism of resistance
A
  • Examples
    • Ciprofloxacin, norfloxacin, levofloxacin, ofloxacin, sparfloxacin, moxifloxacin, gemifloxacin, enoxacin (fluoroquinolones), nalidixic acid (a quinolone).
  • Mechanism
    • Inhibit DNA gyrase (topoisomerase II) and topoisomerase IV.
    • Bactericidal.
    • Must not be taken with antacids.
  • Clinical use
    • Gram-negative rods of urinary and GI tracts (including Pseudomonas), Neisseria, some gram-positive organisms.
  • Toxicity
    • GI upset, superinfections, skin rashes, headache, dizziness.
    • Less commonly, can cause tendonitis, tendon rupture, leg cramps, and myalgias.
    • Contraindicated in pregnant women, nursing mothers, and children under 18 years old due to possible damage to cartilage.
    • Some may cause prolonged QT interval.
    • May cause tendon rupture in people > 60 years old and in patients taking prednisone.
    • Fluoroquinolones** hurt attachments to your bones.**
  • Mechanism of resistance
    • Chromosome-encoded mutation in DNA gyrase, plasmid-mediated resistance, efflux pumps.
20
Q

Metronidazole

  • Mechanism
  • Clinical use
  • Toxicity
A
  • Mechanism
    • Forms free radical toxic metabolites in the bacterial cell that damage DNA.
    • Bactericidal, antiprotozoal.
  • Clinical use
    • Treats Giardia, Entamoeba, Trichomonas, Gardnerella vaginalis, Anaerobes (Bacteroides, C. difficile).
      • Used with a proton pump inhibitor and clarithromycin for “triple therapy” against H. Pylori.
      • GET GAP on the Metro with metronidazole.
    • Treats anaerobic infection below the diaphragm vs. clindamycin (anaerobic infections **above **diaphragm).
  • Toxicity
    • Disulfiram-like reaction (severe flushing, tachycardia, hypotension) with alcohol; headache, metallic taste.
21
Q

Antimycobacterial drugs

  • For each
    • Prophylaxis
    • Treatment
  • M. tuberculosis
  • M. avium–intracellulare
  • M. leprae
A
  • M. tuberculosis
    • Prophylaxis: Isoniazid
    • Treatment: Rifampin, Isoniazid, Pyrazinamide, Ethambutol
      • RIPE for treatment.
  • M. avium–intracellulare
    • Prophylaxis: Azithromycin, rifabutin
    • Treatment:
      • More drug resistant than M. tuberculosis.
      • Azithromycin or clarithromycin + ethambutol.
      • Can add rifabutin or ciprofloxacin.
  • M. leprae
    • Prophylaxis: N/A
    • Treatment:
      • Long-term treatment with dapsone and rifampin for tuberculoid form.
      • Add clofazimine for lepromatous form.
22
Q

Isoniazid (INH)

  • Mechanism
  • Clinical use
  • Toxicity
A
  • Mechanism
    • Decrease synthesis of mycolic acids.
    • Bacterial catalase-peroxidase (encoded by KatG) needed to convert INH to active metabolite.
  • Clinical use
    • Mycobacterium tuberculosis.
    • The only agent used as solo prophylaxis against TB.
    • Different INH half-lives in fast vs. slow acetylators.
  • Toxicity
    • Neurotoxicity, hepatotoxicity.
    • Pyridoxine (vitamin B6) can prevent neurotoxicity, lupus.
    • INH Injures Neurons and Hepatocytes.
23
Q

Rifamycins

  • Examples
  • Mechanism
  • Clinical use
  • Toxicity
  • Other
A
  • Examples
    • Rifampin, rifabutin
  • Mechanism
    • Inhibits DNA-dependent RNA polymerase.
  • Clinical use
    • 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 (increased P-450)
    • Orange body fluids (nonhazardous side effect).
    • Rifabutin favored over rifampin in patients with HIV infection due to less cytochrome P-450 stimulation.
  • Rifampin’s 4 R’s:
    • RNA polymerase inhibitor
    • Ramps up microsomal cytochrome P-450
      • Rifampin ramps up cytochrome P-450, but rifabutin does not
    • ​Red/orange body fluids
    • Rapid resistance if used alone
24
Q

Pyrazinamide

  • Mechanism
  • Clinical use
  • Toxicity
A
  • Mechanism
    • Mechanism uncertain.
    • Thought to acidify intracellular environment via conversion to pyrazinoic acid.
    • Effective in acidic pH of phagolysosomes, where TB engulfed by macrophages is found.
  • Clinical use
    • Mycobacterium tuberculosis.
  • Toxicity
    • Hyperuricemia, hepatotoxicity.
25
Q

Ethambutol

  • Mechanism
  • Clinical use
  • Toxicity
A
  • Mechanism
    • Decreases carbohydrate polymerization of mycobacterium cell wall by blocking arabinosyltransferase.
  • Clinical use
    • Mycobacterium tuberculosis.
  • Toxicity
    • Optic neuropathy (red-green color blindness).
26
Q

Antimicrobial prophylaxis

  • Endocarditis with surgical or dental procedures
  • Gonorrhea
  • History of recurrent UTIs
  • Meningococcal infection
  • Pregnant woman carrying group B strep
  • Prevention of gonococcal or chlamydial conjunctivitis in newborn
  • Prevention of postsurgical infection due to S. aureus
  • Prophylaxis of strep pharyngitis in child with prior rheumatic fever
  • Syphilis
A
  • Endocarditis with surgical or dental procedures
    • Penicillins
  • Gonorrhea
    • Ceftriaxone
  • History of recurrent UTIs
    • TMP-SMX
  • Meningococcal infection
    • Ciprofloxacin (drug of choice), rifampin for children
  • Pregnant woman carrying group B strep
    • Ampicillin
  • Prevention of gonococcal or chlamydial conjunctivitis in newborn
    • Erythromycin ointment
  • Prevention of postsurgical infection due to S. aureus
    • Cefazolin
  • Prophylaxis of strep pharyngitis in child with prior rheumatic fever
    • Oral penicillin
  • Syphilis
    • Benzathine penicillin G
27
Q

Prophylaxis in HIV patients

  • For each
    • Prophylaxis
    • Infection
  • CD4 < 200 cells/mm3
  • CD4 < 100 cells/mm3
  • CD4 < 50 cells/mm3
A
  • CD4 < 200 cells/mm3
    • Prophylaxis: TMP-SMX
      • Aerosolized pentamidine may be used if patient is unable to tolerate TMP-SMX, but this may not prevent toxoplasmosis infection concurrently
    • Infection: Pneumocystis pneumonia
  • CD4 < 100 cells/mm3
    • Prophylaxis: TMP-SMX
      • Aerosolized pentamidine may be used if patient is unable to tolerate TMP-SMX, but this may not prevent toxoplasmosis infection concurrently
    • Infection: Pneumocystis pneumonia and toxoplasmosis
  • CD4 < 50 cells/mm3
    • Prophylaxis: Azithromycin
    • Infection: Mycobacterium avium complex
28
Q

Treatment of highly resistant bacteria

  • MRSA
  • VRE
A
  • MRSA
    • Vancomycin
    • Daptomycin
    • Linezolid (can cause serotonin syndrome)
    • Tigecycline
    • Ceftaroline
  • VRE
    • Linezolid
    • Streptogramins (quinupristin/dalfopristin)

First Aid (92 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions