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BFOM Exam 3 > Antibacterial Agents & Resistance > Flashcards

Antibacterial Agents & Resistance Flashcards

1
Q

Discuss the origin of antimicrobials

A
  • Salvarsan documented 1st antimicrobial = antisyphilitic
  • Sulfonamide is first sulfa drug - competitive inhibitor to para-aminobenzoic acid (folate metabolism)
  • Alexander Fleming notified no staph colonies around penicillin in culture - Chain and Florey isolated compound
  • Prontosil Drug
  • Waksman isolated streptomycin from soil bacteria (Streptomyces griseus)
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2
Q

Explain the concept of selective toxicity and its relationship to antimicrobial agents

A
  • antibiotics cause greater harm to microorganisms than human host
  • expressed as a therapeutic index
    • lowest dose toxic to patient divided by dose typically used for treatment –> lower therapeutic index = less toxic to patient
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3
Q

Discuss the desired antimicrobial properties and pharmacologic activities of antimicrobial agents

A
  • inhibit growth or kill bacterium
  • narrow or broad spectrum
    - con of broad-spectrum = kill off normal flora
  • Negatives
    - antimicrobial resistance
    - suppresion of normal flora
    - allergic reactions
    - toxic effects
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4
Q

Explain the roles of bacterial chromosomal mutations, plasmids, transposons and integrons in the generation of antibiotic resistance mechanisms

A

Mutations: spontaneous, not very effective with drugs that have multiple targets
Plasmids: provides stability, transmissibility; carry multiple resistance cassettes
Transposons:
Integrons:

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5
Q

Describe the major mechanisms of bacterial resistance to antibiotics

A
  • Mycoplasma has no cell wall
  • Mycobacterium has impermeable waxy coat
  • chlamydia, rickettsia, brucella, legionella - live in host cells
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6
Q

What is a bacteriostatic drug? And why use them?

A
  • inhibits growth

- relies on host immunity to eliminate pathogen

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7
Q

What is a bactericidal drug?

A

kills the bacteria

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8
Q

Semisynthetic drugs

A
  • alteration of drug structure to give new properties
  • Penicillin G altered to make ampicillin
  • broadened spectrum of antimicrobial effect
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9
Q

What is a synergistic drug interaction?

A

one drug enhances another

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10
Q

What is an antagonsistic drug interaction?

A

one drug interferes with another

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11
Q

What is a vertical evolution?

A

spontaneous gene mutation (antibiotic resistance)

-low rate

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12
Q

How is mycoplasma resistant to antibiotics?

A

no cell wall

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13
Q

How is mycobacterium resistant to antibiotics?

A

impermeable wax coating

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14
Q

What bacteria live in host cells and therefore are resistant to antibiotics?

A

Chlamydia, Rickettsia, Brucella, Legionella

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15
Q

Mechanisms to resist antibiotics?

A
  • drug inactivation
  • alteration of drug molecule (Penicillin Binding Protein)
  • decreased uptake of the drug
  • increased elimination of the drug
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16
Q

Describe beta-lactams regarding chemical structure, mechanism of action, spectrum of activity, clinical use, and resistance mechanisms

A
  • all bind PBP (responsible for cross-linking petides in proteoglycan synthesis)
  • all types have B-lactam rings (square, 3Cs, 1 N)
  • low oral bioavailability, cannot pass thru BBB due to polarity
  • ineffective against intracellular organisms
  • excreted in urine
  • carbapenam has broadest spectrum
  • chephalosporins is more potent against gram (-)s than penicillin
17
Q

Describe beta-lactamase inhibitors regarding chemical structure, mechanism of action, spectrum of activity, clinical use, and resistance mechanisms

A

-named after the substrate

-

18
Q

Describe glycopeptides regarding chemical structure, mechanism of action, spectrum of activity, clinical use, and resistance mechanisms

A
  • large peptides w/ few monosaccharides
  • gram-(+) only; can’t penetrate cell wall of gram (-)
  • binds peptide ends
  • main indication is B-lactam resistant Gram (+) bacteria (MRSA)
  • poorly absorbed in GI tract
  • lactobacilli resist because of unique peptide ends: D-alanyl-D-lactate – VanA, VanB, VanD enables
  • plasmid associated resistance
19
Q

What type of drug target has a high therapeutic index?

A

cell wall synthesis –> we don’t have cell walls

20
Q

Describe cephalosporins

A
  • beta-lactase
  • chemical structure makes them resistant to beta-lactamases
  • low affinity for gram-(+) bacteria
21
Q

Describe carbapenems

A
  • very resistant to B-lactamases
  • effective against a wide range of gram (+) and (-)organisms
  • can be given to patients with penicillin allergy
22
Q

Describe monobactams

A
  • very resistant to beta-lactamases
  • primarily effective against enterobaccteriaceae
  • can be given to patients with penicillin allergy
23
Q

Describe monobactams

A
  • very resistant to beta-lactamases
  • primarily effective against enterobaccteriaceae
  • can be given to patients with penicillin allergy
24
Q

Explain the advantages and clinical use of semisynthetic penicillins (oxacillin, cloxacillin, ampicillin, and amoxicillin)

A
  • you can change the side group to make the drug more bioavailable and have a broader spectrum
  • 3 goals: acid stability, B-lactamase resistance, extended spectrum
25
Q

Discuss the mechanism of action, clinical use, and spectrum of activity of polypeptide antibiotics

A

Bacitracin
-inhibit dephosphorylation & recycling of bactoprenol
-damage cytoplasmic membrane & inhibit transcription
-low therapeutic index – only use topicaly
Polymyxins
-cyclic polypeptides
-insert into membranes to increase cell permeability
-most effective against gram (-)s
-nephrotoxicity – topical application only

26
Q

Compare and contrast antibacterial agents that interfere with protein synthesis regarding chemical structure, mechanism of action, spectrum of activity, clinical use, and resistance mechanisms

A

Aminoglycosides
-irreversibly bind 30S subunit –> distortion & malfunction, blocks transcription
-not effective against anaerobes, enterococci, and streptococci
-in combo with B-lactam drugs – more permeability
-low oral bioavailability
-use for severe life-threatening gram (-) infections
-side effects: nephrotoxicity & ototoxicity
-resistance through modifying proteins and alteration of ribosomal target
Tetracyclines
-reversibly bind 30S subunit –> block attachment of tRNA, prevents protein elongation
-effective against gram-(+) and (-)
-resistance due to decreased penetration into cell, active efflux out of cell (transposon mediated), alteration of ribosomal target, enzymatic modification of drug
Macrolides
-reversibly bind to 50S subunit –> prevents continuation of protein synthesis
-good GI absorption, wide distribution
-effective against gram (+), some gram (-) coccobacilli and intracellular bacteria
-for patients allergic to penicillin
-resistance due to methylation of 50S subunit, enzymatic modification of drug, efflux of antibiotic

27
Q

Discuss cross-resistance between macrolides, lincosamides, and streptogramins

A

-due to methylated 50S ribosome

28
Q

Discuss antibacterial agents that interfere with nucleic acid synthesis regarding chemical structure, mechanism of action, spectrum of activity, clinical use, and resistance mechanisms

A

Quinolones

  • inhibit action of topoisomerase DNA gyrase
  • effective against gram (+) and gram (-)
  • resistance due to alteration of DNA gyrase, altered uptake, and efflux (all due to a mutation)
29
Q

Explain the mechanisms of synergism between sulfonamides and trimethoprim

A

-metabolic pathway inhibitors
-inhibit prooduction of folic acid
Sulfonamides
-sulfa drug family
-inhibit growth of gram-(+) and (-)s – competitive inhibition
-structurally similar to para-aminobenzoic acid in folate pathway (humans don’t have this enzyme)
-resistance due to plasmid
Trimethoprim
-inihibits dihydrofolate reductase
-resistance due to plasma encoded alternative enzyme

30
Q

Discuss antibacterial agents for treating M. tuberculosis infection regarding regarding chemical structure, mechanism of action, spectrum of activity, clinical use, and resistance mechanisms

A

Rifampin
Streptomycin
Isoniazid –> inihibits synthesis of mycolic acid
Ethambutol –> inihibits arabinogalactan synthesis in cell wall
Pyrazinamide –> disrupts proton motive force; inhibits FAS1
-resistance due to chromosomal gene mutations
-these first line drugs have low toxicity

BFOM Exam 3 (19 decks)

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