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Medical Microbiology > Antimicrobial Agents > Flashcards

Antimicrobial Agents Flashcards

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Biology 101 flashcards USMLE® Step 1 flashcards
1
Q

Bacteriostatic

A

prevents bacterial growth/division

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2
Q

Bactericide

A

kills bacteria

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3
Q

Selective toxicity

A

Efficient against the bacteria, but low toxicity for the

patient

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4
Q

Mechanisms of resistance

A
  • Target modification
  • Reduced permeability
  • Reduced access to target
  • Active efflux
  • Enzymatic inactivation or modification
  • Alternative pathways
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5
Q

Penicillin

A
  • Inhibits bacterial cell wall synthesis
  • Very efficient against Gram-positive bacteria
  • Low production cost
  • Low toxicity for humans
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6
Q

Penicillin resistance

A

b-lactamases

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7
Q

b-lactamases

A
  • Secreted in Gram+
  • Periplasm in Gram-
  • inhibited by: Clavulanic acid, Sulbactam, Tazobactam
  • new are not bound by inhibitors
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8
Q

Methicillin

A
  • New penicillin derivative
  • Resistant to the new b-lactamases
  • New PBP
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9
Q

β-lactam resistance – Gram+

A
  • Target modification

- Enzymatic inactivation or modification

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10
Q

β-lactam resistance – Gram-

A
  • Target modification
  • Enzymatic inactivation or modification
  • Reduced permeability
  • Reduced access to target
  • Active efflux
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11
Q

β-lactams

A
  • Penicillins
  • Cephalosporins
  • Monobactams
  • Cephamycins
  • Carbapenems
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12
Q

Cephalosporins

A
  • 1st generation: narrow spectrum
  • 2nd generation: expanded spectrum
  • 3rd generation: broad spectrum
  • 4th generation: extended spectrum
  • 5th generation: activity against MRSA
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13
Q

MRSA

A

Methicillin-resistant Staphylococcus aureus

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14
Q

Glycopeptides

A
  • Parenteric
  • Large molecules – unable to enter Gram-
  • Prevent peptidoglycan synthesis by interacting with D-Ala-D-Ala termini, inhibiting PBP activity.
  • Intrinsic resistance in species with D-Ala-D-Lac or D-Ala-D-Ser termini
  • Acquired resistance by modification of the D-Ala-D-Ala terminal – van genes located in plasmids and transposons (Enterococcus) – detected in MRSA!
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15
Q

Glycopeptide resistance

A

Alternative pathways

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16
Q

Other inhibitors of cell wall synthesis

A
  • Bacitracin: membrane carrier molecules that transport the building-blocks of the peptidoglycan bacterial cell wall
  • Fosfomycin: inactivating the enzyme UDP-N acetylglucosamine-3 enolpyruvyltransferase, also known as MurA
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17
Q

Inhibition of protein synthesis

A

Ribossomes:

  • Prokaryotes 70S (50S + 30S)
  • Eukaryotes 80S (60S + 40S)
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18
Q

Aminoglycosides

A
  • Irreversibly bind to the 30S sub-unit
  • Streptomycin, gentamicin, amikacin, tobramycin
  • Bactericidal
  • Serious infections caused by Gram- rods and some Gram+
  • Frequently administered in association with inhibitor of cell wall synthesis
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19
Q

Aminoglycosides resistance

A
  • Resistance in anaerobes or aerobes in anerobic environment
  • Resistance in streptococci and enterococci
  • Enzymatic inactivation or modification
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20
Q

Tetracyclines

A
  • Tetracycline, doxycycline, minocycline
  • Reversibly bind to the 30S sub-unit (bacteriostatic)
  • Blocks docking site of tRNA, preventing peptide chain
    elongation
21
Q

Tetracyclines resistance

A

Active efflux

22
Q

Chloramphenicol

A
  • Reversibly binds to the peptidyltransferase component of the 50S sub-unit (bacteriostatic)
  • Prevents peptide chain elongation
  • Limited use because it disrupts protein synthesis in human bone marrow cells - blood dyscrasias
23
Q

Chloramphenicol resistance

A

Enzymatic inactivation or modification

24
Q

Macrolides and lincosamides

A
  • Most Gram- bacteria are resistant to macrolides

- Clindamycin is active against anaerobic Gram- rods

25
Q

Macrolide resistance

A
  • Active efflux

- Target modification

26
Q

M phenotype

A
  • Resistance to 14- and 15-member macrolides mef genes (efflux pumps)
  • Active efflux
27
Q

cMLSB phenotype

A
  • Resistance to all macrolides, lincosamides and streptogramin B
  • erm genes
  • rRNA methylation
28
Q

iMLSB phenotype

A
  • rRNA methylation
  • Resistance to all macrolides, lincosamides and streptogramin B in presence of macrolides
  • erm genes
29
Q

Quinolones

A
  • Inhibition of nucleic acid synthesis
  • preventing bacterial DNA from unwinding and duplicating
  • inhibit the ligase activity
30
Q

Quinolone resistance

A
  • Target modification
  • Reduced access to target
  • Reduced permeability
  • Active efflux
31
Q

Antimetabolites

A
  • Sulfonamides
  • Trimethoprim
  • affect purine and pyrimidine formation
  • Synergistic effect
32
Q

Antimetabolites resistance

A
  • Intrinsic resistance in bacteria that use exogenous thymidine (e.g., enterococci)
  • Acquired resistance to trimethoprim due to production of alternative dihydrofolate reductase with low afinity for
    trimethoprim
33
Q

Rifampin (=Rifampicin)

A
  • Binds DNA-dependent RNA polymerase and inhibits the
    initiation of RNA synthesis
  • Active against aerobic Gram+ cocci and Mycobacterium
  • Instrinsic resistance in Gram- due to decreased uptake
  • Acquired resistance due to mutations in the gene encoding the beta subunit of RNA polymerase
34
Q

Antimycobacterial agents

A
  • Isoniazid: Inhibition of mycolic acids synthesis
  • Ethambutol: Inhibition of arabinogalactan synthesis
  • Pyrazinamide: Unknown mechanism of action
35
Q

Antimicrobial associations

A
  • Synergistic effect
  • Prevent treatment failures due to resistance emergence
  • Treatment of polymicrobial infections
  • Treatment of severe infections before pathogen identification
36
Q

Antifungal agents

A
  • Polyenes
  • Azoles
  • Echinocandins
37
Q

Polyenes

A
  • Amphotericin B:
    Binds ergosterol, forming pores in the membrane
    Binds cholesterol - toxicity in humans
  • Nystatin (Topical agent)
38
Q

Azoles

A
  • Inhibit ergosterol synthesis

- Clotrimazole, Ketoconazole, Fluconazole, Voriconazole, Posaconazole

39
Q

Echinocandins

A
  • Inhibit glucan synthesis
  • Specific toxicity against fungi with 1,3-β-glucan as the main glucan
  • Caspofungin, Micafungin
40
Q

Flucytosine

A
  • Antimetabolite (nucleotide analogous): interferes with the synthesis of DNA, RNA, and proteins
  • Combination with amphotericin B or fluconazole due to the propensity for resistance emergence
41
Q

Griseofulvin

A

Interacts with microtubules -Inhibition of mitosis

42
Q

Terbinafine

A
  • Allylamine: inhibits ergosterol synthesis

- Oral and topical

43
Q

Antifungal resistance

A
  • Antifungal inactivation is not observed
  • Resistance genes are not transmissible from cell to cell
  • Resistance develops slowly
  • Emergence of intrinsically resistant species or gradual,
    stepwise alteration of cellular structures or functions
    following exposure to the antifungal agent
44
Q

Nitroimimidazoles

A
  • Metronidazole
  • Anaerobic bacteria and protozoa
  • Reduction of the antibiotic (anaerobic metabolism) produces cytotoxic compounds that disrupt the host DNA
  • Resistance due to reduced uptake or elimination of the
    cytotoxic compounds
45
Q

Polymyxins

A
  • Cyclic polypeptides
  • Insert into bacterial membranes, by interacting with lipopolysaccharides and phospholipids in the outer membrane
  • Nephrotoxicity
  • Gram-: Multidrug resistant Klebsiella, Acinetobacter, Pseudomonas
46
Q

Lipopeptides

A
  • Daptomycin

- Tigecycline (Glycylcycline)

47
Q

Daptomycin

A
  • Binds cytoplasmic membrane - Depolarization; disruption of ionic gradients
  • Gram+: Multidrug resistant Staphylococci, Streptococci,
    Enterococci (including vancomycin-resistant)
48
Q

Tigecycline (Glycylcycline)

A
  • Derivative of minocycline
  • Higher binding affinity for the ribosome
  • Less affected by efflux or enzymatic modification

Medical Microbiology (2 decks)

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