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Mirobiology > Antibiotics > Flashcards

Antibiotics Flashcards

1
Q

Penicillin G, V

A

Prototype β-lactam antibiotics (penicillinase-sensitive)

  • Penicilling G → Iv and IM form
  • Penicillin V → oral
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2
Q

Penicillin G, V mechanism

A
  1. Bind penicillin-binding proteins (transpeptidases).
  2. Block transpeptidase cross-linking of peptidoglycan in cell wall.
  3. Activate autolytic enzymes.
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3
Q

Penicillin G,V clinical use

A
  1. ​Mostly used for gram-positive organisms
    1. S. pneumoniae
    2. S. pyogenes
    3. Actinomyces
  2. Gram negative cocci
    1. N. meningitidis
  3. Spirochetes
    1. T. pallidum

Bactericidal for gram-positive cocci, gram-positive rods, gram-negative cocci, and spirochetes.

Penicillinase sensitive.

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4
Q

Penicilling G, V toxicity

A
  • Hypersensitivity reactions
  • Hemolytic anemia
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5
Q

Penicillin G, V resistance

A

Penicillinase in bacteria (a type of β-lactamase) cleaves β-lactam ring.

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6
Q

Aminopenicillins

A
  • ​amoxicillin
  • ampicllin

Penicillinase-sensitive penicillins

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7
Q

Aminopenicillin mechanism

A
  • Same as penicillin → wider spectrum,
  • Penicillinase sensitive.
  • Also combine with clavulanic acid to protect against destruction by β-lactamase.

(amoxicillin and ampicillin)

Note that amoxicillin has greater oral bioavailability than ampicllin.

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8
Q

Aminopenicillin clinical use

A

Exteneded spectrum penicillin

  1. H. influenzae (gram negative)
  2. H. pylori (gram negative, oxidase positive, comma shaped)
  3. E. coli (gram negative rod)
  4. Listeria monocytogenes (gram positive rod)
  5. Proteus mirabilis (gram negative rod)
  6. Salmonella (gram negative rod)
  7. Shigella (gram negative rod)
  8. enterococci (gram positive cocci)
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9
Q

Aminopenicillin toxicity

A
  • hypersensitivity reactions
  • rash
  • pseudomembranous colitis (ie C. dif, a gram positive rod)
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10
Q

Aminopenicillin resistance

A

Penicillinase in bacteria (a type of β-lactamase) cleaves β-lactam ring.

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11
Q

Penicillinase-resistant penicillins

A
  1. Dicloxacillin
  2. Nafcillin
  3. Oxacillin
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12
Q

Penicillinase resistant penicillins mechanism

A

(dicloxacillin, nafcillin, oxacillin)

Same as penicillin → narrow spectrum.

Penicillinase resistant because bulky R group blocks access of β-lactamase to β-lactam ring.

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13
Q

Penicillinase resistant penicillins clinical use

A

(dicloxacillin, nafcillin, oxacillin)

S. aureus (except MRSA; resistant because of altered penicillin-binding protein target site).

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14
Q

Penicillinase resistant penicillins toxicity

A
  • Hypersensitivity reactions
  • interstitial nephritis
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15
Q

Antipseudomonals

A
  • Piperacillin
  • Ticarcillin
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16
Q

Antipseudomonal mechanism

A

(piperacillin, ticarcillin)

Same as penicillin. Extended spectrum.

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17
Q

Antipseudomonal clinical use

A

(piperacillin, ticarcillin)

Pseudomonas spp. and other gram-negative rods.

Susceptible to penicillinase; use with β-lactamase inhibitors.

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18
Q

Antipseudomonal toxicity

A

(piperacillin, ticarcillin)

Hypersensitivity reactions.

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19
Q

Beta lactamase inhibitors

A
  1. Clavulanic Acid
  2. Sulbactam
  3. Tazobactam

Often added to penicillin antibiotics to protect the antibiotic from destruction by β-lactamase (penicillinase).

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20
Q

Cephalosporins (generations 1-4) mechanism

A

β-lactam drugs that inhibit cell wall synthesis but are less susceptible to penicillinases. Bactericidal.

Organisms typically not covered by cephalosporins are LAME:

  • Listeria
  • Atypicals (Chlamydia, Mycoplasma)
  • MRSA
  • Enterococci

Exception: ceftaroline covers MRSA.

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21
Q

First generation cephalosporins

A
  1. Cefazolin (IV)
  2. cephalexin (oral)
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22
Q

First generation cephalosporin clinical use

A

1st generation (cefazolin, cephalexin)—

  1. gram-positive cocci
  2. gram-negative rods
    1. Proteus mirabilis
    2. E. coli
    3. Klebsiella pneumoniae

Cefazolin used prior to surgery to prevent S. aureus wound infections.

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23
Q

Second generation cephalosporin clinical use

A

2nd generation (cefoxitin, cefaclor, cefuroxime)—

  1. gram-positive cocci
  2. Haemophilus influenzae
  3. Enterobacter aerogenes
  4. Neisseria spp.
  5. Proteus mirabilis
  6. E. coli
  7. Klebsiella pneumoniae
  8. Serratia marcescens
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24
Q

Second generation cephalosporins

A
  1. cefoxitin (IV)
  2. cefaclor
  3. cefuroxime
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25
Q

Third generation cephalosporins

A
  1. ceftriaxone
  2. cefotaxime
  3. ceftazidime
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26
Q

Third generation cephalosporin clinical use

A

3rd generation (ceftriaxone, cefotaxime, ceftazidime)—serious gram-negative infections resistant to other β-lactams.

Ceftriaxone—meningitis, gonorrhea, disseminated Lyme disease (borrelia).

Ceftazidime—Pseudomonas

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27
Q

Fourth generation cephalosporins

A

cefepime

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28
Q

Fourth generation cephalosporin clinical use

A

4th generation (cefepime)—

gram-negative organisms

with ↑ activity against Pseudomonas and gram-positive organisms.

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29
Q

Fifth generation cephalosporins

A

Ceftaroline

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30
Q

Fifth generation cephalosporin clinical use

A

5th generation (ceftaroline)— broad gram-positive and gram-negative organism coverage, including MRSA.

Does not cover Pseudomonas.

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31
Q

Cephalosporin toxicity

A
  1. hypersensitivity reactions
  2. autoimmune hemolytic anemia
  3. disulfiram-like reaction
  4. vitamin K deficiency
  5. Exhibit cross-reactivity with penicillins, ↑ nephrotoxicity of aminoglycosides.
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32
Q

Cephalosporin resistance

A

Structural change in penicillin-binding proteins (transpeptidases).

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33
Q

Carbapenems

A
  1. imipenem
  2. meropenem
  3. ertapenem (limited Pseudomonas coverage)
  4. doripenem
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34
Q

Carbapenem mechanism

A

Imipenem is a broad-spectrum, β-lactamase– resistant carbapenem. Always administered with cilastatin (inhibitor of renal dehydropeptidase I) to ↑ inactivation of drug in renal tubules.

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35
Q

Carbapenem clnical use

A

(imipenem, meropenem, ertapenem, doripenem)

  • ​Gram-positive cocci
  • Gram-negative rods
  • Anaerobes

Wide spectrum, but significant side effects limit use to life-threatening infections or after other drugs have failed.

Meropenem has a ↓ risk of seizures and is stable to dehydropeptidase I.

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36
Q

Carbapenem toxicity

A
  • GI distress
  • skin rash,
  • CNS toxicity (seizures) at high plasma levels
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37
Q

Monobactams

A

Aztreonam

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38
Q

Monobactam mechanism

A

Prevents peptidoglycan cross-linking by binding to penicillin- binding protein 3.

  • Less susceptible to β-lactamases.
  • Synergistic with aminoglycosides.
  • No cross-allergenicity with penicillins.
39
Q

Monobactam clinical use

A

Gram-negative rods only—no activity against gram-positives or anaerobes.

For penicillin-allergic patients and those with renal insufficiency who cannot tolerate aminoglycosides.

40
Q

Monobactam toxicity

A

Usually nontoxic; occasional GI upset.

41
Q

Glycopeptides

A
  • Bacitracin
  • Vancomycin
42
Q

Vancomycin mechanism

A

Inhibits cell wall peptidoglycan formation by binding D-ala D-ala portion of cell wall precursors.

Bactericidal. Not susceptible to β-lactamases.

43
Q

Vancomycin clinical use

A

Gram-positive bugs only—serious, multidrug-resistant organisms, including

  • MRSA
  • S. epidermidis
  • sensitive Enteroccocus species
  • Clostridium difficile (oral dose for pseudomembranous colitis)
44
Q

Vancomycin toxicity

A

Well tolerated in general—but NOT trouble free.

  1. Nephrotoxicity
  2. Ototoxicity
  3. Thrombophlebitis
  4. diffuse flushing—red man syndrome (can largely prevent by pretreatment with antihistamines and slow infusion rate)
45
Q

Vancomycin resistance

A

Occurs in bacteria via amino acid modification of D-ala D-ala to D-ala D-lac.

46
Q

Aminoglycosides

A
  1. Gentamicin
  2. Neomycin
  3. Amikaein
  4. Tobramycin
  5. Streptomycin
47
Q

Aminoglycoside mechanism

A

Bactericidal.

Irreversible inhibition of initiation complex through binding of the 30S subunit. Can cause misreading of mRNA. Also block translocation.

Require O2 for uptake; therefore ineffective against anaerobes.

48
Q

Aminoglycoside clinical use

A

Severe gram-negative rod infections. Synergistic with β-lactam antibiotics.

Neomycin for bowel surgery.

49
Q

Aminoglycoside toxicity

A
  1. Nephrotoxicity
  2. Neuromuscular blockade
  3. Ototoxicity (especially when used with loop diuretics)
  4. Teratogen.
50
Q

Aminoglycoside resistance

A

Bacterial transferase enzymes inactivate the drug by

  • acetylation
  • phosphorylation
  • or adenylation
51
Q

Tetracyclines

A
  1. Tetracycline
  2. Doxycycline
  3. Minocycline
52
Q

Tetracycline mechanism

A

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 tetracyclines with

  • milk (Ca2+),
  • antacids (Ca2+ or Mg2+),
  • or iron-containing preparations

because divalent cations inhibit drugs’ absorption in the gut.

53
Q

Tetracycline clinical use

A
  • Borrelia burgdorferi
  • M. pneumoniae

Drugs’ ability to accumulate intracellularly makes them very effective against Rickettsia and Chlamydia. Also used to treat acne.

54
Q

Tetracycline toxicity

A
  1. GI distress
  2. discoloration of teeth
  3. inhibition of bone growth in children
  4. photosensitivity
  5. Contraindicated in pregnancy.
55
Q

Tetracycline resistance

A

↓ uptake or ↑ efflux out of bacterial cells by plasmid-encoded transport pumps.

56
Q

Chloramphenicol mechanism

A

Blocks peptidyltransferase at 50S ribosomal subunit. Bacteriostatic.

57
Q

Chloramphenicol clinical use

A

Meningitis

  • Haemophilus influenzae
  • Neisseria meningitidis
  • Streptococcus pneumoniae

Rocky Mountain spotted fever

  • Rickettsia rickettsii

Limited use owing to toxicities but often still used in developing countries because of low cost.

58
Q

Chloramphenicol toxicity

A
  1. Anemia (dose dependent)
  2. aplastic anemia (dose independent)
  3. gray baby syndrome (in premature infants because they lack liver UDP-glucuronyl transferase).
59
Q

Chloramphenicol mechanism of resistance

A

Plasmid-encoded acetyltransferase inactivates the drug.

60
Q

Lincosamide

A

Clindamycin

61
Q

Clindamycin mechanism

A

Blocks peptide transfer (translocation) at 50S ribosomal subunit. Bacteriostatic.

62
Q

Clindamycin clinical use

A

Anaerobic infections (e.g.,

  • Bacteroides spp.
  • Clostridium perfringens

in

  • aspiration pneumonia
  • lung abscesses
  • oral infections.

Also effective against invasive group A streptococcal infection (strep pyogenes).

[Treats anaerobic infections above the diaphragm vs. metronidazole (anaerobic infections below diaphragm)]

63
Q

Clindamycin Toxicity

A
  1. Pseudomembranous colitis (C. difficile overgrowth)
  2. fever
  3. diarrhea
64
Q

Oxazolidinones

A

Linezolid

65
Q

Oxazolidinones mechanism

A

Inhibit protein synthesis by binding to 50S subunit and preventing formation of the initiation complex.

66
Q

Oxazolidinones clinical use

A

Gram-positive species including MRSA and VRE

67
Q

Oxazolidinones toxicity

A
  1. Bone marrow suppression (especially thrombocytopenia)
  2. peripheral neuropathy
  3. serotonin syndrome
68
Q

Oxazolidinones resistance

A

Point mutation of ribsomal RNA.

69
Q

Macrolides

A
  1. Azithromycine
  2. Clarithomycin
  3. Erythromycin
70
Q

Macrolide mechanism

A

(Azithromycin, clarithromycin, erythromycin)

Inhibit protein synthesis by blocking translocation; bind to the 23S rRNA of the 50S ribosomal subunit. Bacteriostatic.

71
Q

Macrolide clinical use

A
  1. Atypical pneumonias
    1. Mycoplasma
    2. Chlamydia
    3. Legionella
  2. STIs
    1. Chlamydia
  3. gram-positive cocci
    1. streptococcal infections in patients allergic to penicillin
  4. B. pertussis
72
Q

Macrolide toxicity

A
  1. Gastrointestinal motility issues
  2. Arrhythmia caused by prolonged QT interval
  3. acute cholestatic hepatitis
  4. rash
  5. eosinophilia.
  6. Increases serum concentration of theophyllines, oral anticoagulants.
  7. Clarithromycin and erythromycin inhibit cytochrome P-450.
73
Q

Macrolide resistance

A

Methylation of 23S rRNA-binding site prevents binding of drug

74
Q

Floroquinolones

A
  1. Ciprofloxacin
  2. norfloxacin
  3. levofloxacin
  4. ofloxacin
  5. moxifloxacin
  6. gemifloxacin
  7. enoxacin
75
Q

Floroquinolone mechanism

A

Inhibit prokaryotic enzymes topoisomerase II (DNA gyrase) and topoisomerase IV.

Bactericidal. Must not be taken with antacids.

76
Q

Floroquinolone clinical use

A
  • Gram-negative rods of urinary and GI tracts (including Pseudomonas)
  • Neisseria
  • some gram-positive organisms
77
Q

Floroquinolone toxicity

A
  1. GI upset
  2. superinfections
  3. skin rashes
  4. headache
  5. dizziness
  6. Less commonly, can cause leg cramps and myalgias.
  7. Contraindicated in pregnant women, nursing mothers, and children < 18 years old due to possible damage to cartilage.
  8. Some may prolong QT interval.
  9. May cause tendonitis or tendon rupture in people > 60 years old and in patients taking prednisone.
78
Q

Floroquinolone resistance

A
  1. Chromosome-encoded mutation in DNA gyrase
  2. plasmid-mediated resistance
  3. efflux pumps
79
Q

Lipopeptide

A

Daptomycin

80
Q

Daptomycin mechanism

A

Lipopeptide that dirsupts cell membcane of gram-positive cocci.

81
Q

Daptomycin clinical use

A
  1. S. aureus skin infections (especially MRSA)
  2. bacteremia
  3. endocarditis
  4. VRE (vancomycin resistant eneterococcus)

Not used for pneumonia (avidly binds to and is inactivated by surfactant).

82
Q

Daptomycin toxicity

A
  • Myopathy
  • rhabdomyolysis
83
Q

Nitroimidazole

A

Metronidazole

84
Q

Metronidazole mechanism

A

Forms toxic free radical metabolites in the bacterial cell that damage DNA.

Bactericidal, antiprotozoal.

85
Q

Metronidazole clinical use

A

Treats

  1. Giardia
  2. Entamoeba
  3. Trichomonas
  4. Gardnerella vaginalis
  5. Anaerobes
    1. Bacteroides
    2. C. difficile

Used with a proton pump inhibitor and clarithromycin for “triple therapy” against H. Pylori.

Treats anaerobic infection below the diaphragm vs. clindamycin (anaerobic infections above diaphragm).

86
Q

Metronidazole toxicity

A
  1. Disulfiram-like reaction with alcohol
    1. severe flushing
    2. tachycardia
    3. hypotension
  2. headache
  3. metallic taste
87
Q

Sulfonamides

A
  1. ​Sulfamethoxazole (SMX) (short acting)
  2. Sulfisoxazole (topical)
  3. Sulfadiazine (short acting)
88
Q

Sulfonamide mechanism

A

Inhibit folate synthesis. Para-aminobenzoic acid (PABA) antimetabolites inhibit dihydropteroate synthase.

Bacteriostatic (bactericidal when combined with trimethoprim).

(Dapsone, used to treat lepromatous leprosy, is a closely related drug that also inhibits folate synthesis.)

89
Q

Sulfonamide clinical use

A
  1. Gram-positives
  2. gram-negatives
  3. Nocardia
  4. Chlamydia
  5. Triple sulfas or SMX for simple UTI
90
Q

Sulfonamide toxicity

A
  1. Hypersensitivity reactions
  2. hemolysis if G6PD deficient
  3. nephrotoxicity (tubulointerstitial nephritis)
  4. photosensitivity
  5. kernicterus in infants
  6. displace other drugs from albumin (e.g., warfarin)
91
Q

Sulfonamide resistance

A

Altered enzyme (bacterial dihydropteroate synthase), ↓ uptake, or ↑ PABA synthesis.

92
Q

Trimethoprim mechanism

A

Inhibits bacterial dihydrofolate reductase.

Bacteriostatic.

93
Q

Trimethoprim clinical use

A

Used in combination with sulfonamides (trimethoprim-sulfamethoxazole [TMP- SMX]), causing sequential block of folate synthesis.

Combination used for

  1. UTIs
  2. Shigella
  3. Salmonella
  4. Pneumocystis jirovecii pneumonia treatment and prophylaxis
  5. toxoplasmosis prophylaxis
94
Q

Trimethoprim toxicity

A
  1. Megaloblastic anemia
  2. leukopenia
  3. granulocytopenia

(May alleviate with supplemental folinic acid)

Mirobiology (1 decks)

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