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Microbiology > Exam #1: Antibiotics > Flashcards

Exam #1: Antibiotics Flashcards

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Biology 101 flashcards
1
Q

What is the principle of selective toxicity?

A

Killing microorganism w/out harming the host

- Dependent on biochemical differences between the two e.g. ribosomes

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2
Q

What is an Antibiotic?

A

Natural antibiotic produced in nature

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3
Q

What is an antimicrobial Antimicrobial?

A

Antibiotic synthesized in a lab

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4
Q

Define Bacteriostatic.

A

Inhibits growth of bacteria, but does NOT kill the bacteria

- Used in immunocompetent & mild infection

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5
Q

Define Bactericidal.

A

Kills bacteria

- Used in immunocompromised & severe infections

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6
Q

Define Antibiotic Synergism.

A

Combination of two antibiotics leads to enhanced bactericidal activity

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7
Q

Define Antibiotic Antagonism.

A

Combination of two antibiotics, where one interferes with the other

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8
Q

What does it mean to say that an antibiotic is “Broad Spectrum?” What are the advantages & disadvantages of broad spectrum antibiotics?

A

Effective against a large variety of bacteria

  • Advantage= increased likelihood of efficacy when unknown etiology
  • Disadvantage= may disrupt patient’s normal host micobiota
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9
Q

What does it mean to say that an antibiotic is “Narrow Spectrum?” What are the advantages & disadvantages of narrow spectrum antibiotics?

A

Target a small subset of bacteria

  • Advantage= avoid effects to microbiota
  • Disadvantage= must have specific disease causing bacteria identified & choose correct antibiotic
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10
Q

Describe the principle of antibiotic resistance. What causes antibiotic resistance?

A
  • Antibiotics DO NOT cause resistance; genetic mutation or acquisition of genetic elements from other bacteria carrying resistance genes may result in antibiotic resistance
  • Antibiotics select against sensitive bacteria & consequently allow for the survival of bacteria that have gained a rare mutation
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11
Q

When you see a lab report on a bacterial culture, what do S, I, & R mean?

A

S= sensitive, may be treated w/ dosage regimen & antimicrobial recommended

I= intermediate, infection may be treated at sites where antibiotic can be concentrated or a high dose can be tolerated

R= resistant, resistant isolates are NOT inhibited by the usually achieved concentrations of antimicrobials

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12
Q

Why is it bad to stop antibiotics early?

A
  • Antibiotic kills sensitive bacteria & consequently selects for more resistant bacteria
  • Normally these are killed by the host & dampended by continued antibiotic use
  • Non-compliance leads to worse–more resistant infection–that can be spread to others
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13
Q

What are the principles of rational & effective antibiotic utilization?

A
  • Antibiotics are only useful for treating bacterial infection
  • Before treatment, gain a representative sample & then treat
  • Empiric therapy= treatment w/ broad spectrum while waiting for lab results
  • Targeted therapy= refined/ narrow spectum after lab results
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14
Q

What are the three groups of patients that receive prophylactic antibiotics?

A

1) Immunocompormised
2) Surgical to prevent nosocomial infections (hospital acquired)
3) Exposure to high risk pathogens

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15
Q

How do bacteria resist antibiotics?

A

1) Breakdown of the antibiotic via hydrolysis
2) Chemical modification of antibiotic so it is no longer effective
3) Alteration of the antibiotic target
4) Altered permeability via decreased influx or increased efflux of the cell membrane e.g. pumps that literally “pump” the antibiotic out of the cell
5) Lack of target

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16
Q

What does MIC stand for?

A

Minimum inhibitory concentration= lowest concentration of abx that inhibits growth

17
Q

What does MIB stand for?

A

Minimum bactericidal concentration= lowest concentration that kills

18
Q

What are the three ways that MIC can be measured?

A
  • Disk diffusion assay i.e. Kirby-Bauer test, measure the “zone of inhibition” by placing antibiotic discs on a culture plate w/ bacteria
  • E-test= high to low concentration of antibiotics in a strip on a culture plate
  • Broth culture
19
Q

Describe the process of Broth Culture. How are MIC & MIB determined?

A
  • Various test tubes given same number of bacteria, but different concentrations of antibiotics
  • Measure optical density (more density= less light through & more bacteria present)
  • MIC= concentration where you don’t see growth that is right next to the one where you do
  • MIB= measured by plating/ culture & finding the concentration where there is NO growth on the plate (likely higher concentration than MIC)
20
Q

What is the difference between Cell Wall Active & Membrane Active Antibiotics?

A

Cell wall active= disrupt peptidoglycan synthesis
- Only effective against rapidly dividing bacteria but NOT resting bacteria

Membrane active= disrupts the lipid membrane of the bacterial cell
- Effective against resting & actively dividing bacteria

21
Q

What class of antibiotics are Cell Wall Synthesis Inhibitors? What specific antibiotics are contained within this class?

A

B-Lactams

  • PCN
  • Cephalosporins
  • Cephamycins
  • Carbapenems
  • Monobactams
22
Q

Describe the B-Lactam mechanism of action.

A

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23
Q

How do bacteria become resistant to B-Lactams?

A

1) Altered transpeptidase
2) Altered outer membrane permeability
3) Efflux pumps
4) Chemical modification of the antibiotic via B-lactamase–>degradation of the B-lactam so that it no longer binds in the peptidoglycan binding protein pocket

24
Q

Describe the mechanism of action of Vancomycin.

A

Prevents peptidoglycan synthesis by:

1) Binding terminal alanines & covering them
2) Cell wall synthesis cannot occur

25
Q

How do bacteria become resistant to Vancomycin?

A

By replacing terminal D-alanine in the pentapeptide with D-lactate; transpeptidase is still effective in catalyzing reaction to make peptidoglycans

I.e. by altering the target of Vancomycin

26
Q

Describe the mechanism of Bacitracin.

A

In shuttling NAG-NAM-pentapeptide to the outer leaflet of the plasma membrane for peptidoglycan synthesis, bactoprenol is diphosphorylated. It must be dephosphorylated to be recycled back to the inner leaflet. Bacitracin inhibits bactoprenol dephosphorylation/ recycling.

27
Q

What antibiotics are protein synthesis inhibitors?

A
  • Tetracycline
  • Aminoglycosides
  • Macrolides
28
Q

Describe the mechanism of Tetracycline.

A
  • Bacteriostatic
  • Binds 30S subunit
  • Broad spectum

E.g. Tetracycline & Doxycycline

29
Q

Describe the mechanism of Aminoglycosides.

A
  • Bactericidal
  • Binds 30S subunit
  • Oxygen-dependent (will not kill anaerobic bacteria in gut)
  • Narrow-spectrum

E.g. Gentamicin & Kanamycin

30
Q

Describe the mechanism of Macrolides.

A
  • Bacteriostatic
  • Bind 50S subunit
  • Alternative to PCN

E.g. Erythryomycin & Azythromycin

31
Q

Which antibiotics are nucleic acid synthesis inhibitors?

A
  • Quinolones
  • Rifampin & Rifabutin
  • Metronidazole
32
Q

Describe the mechanism of the Quinolones.

A

Inhibits DNA replication, recombination, & repair by inhibiting toposiomerase (DNA gyrase)

33
Q

Describe the mechanism of Rifampin & Ribabutin.

A

Binds DNA-dependent RNA polymerase & inhibits initiation of RNA synthesis

34
Q

Describe the mechanism of Metronidazole.

A

Drug is reduced by bacteria into toxic compounds that damage DNA

35
Q

Which drugs are antimetabolites? What is their mechanism of action?

A
  • Sulfonamides & Trimethoprim

- Inhibition of folate synthesis

Microbiology (49 decks)

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