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micb 308 > Antibiotics > Flashcards

Antibiotics Flashcards

1
Q

how was it proven that Mtb causes disease

A
  • show invasion and multiplication of Mtb using Koch’s Postulates
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2
Q

how was Mtb shown to cause disease using Koch’s Postulate (3)

A
  • isolate the bacilli
  • grow it in pure culture
  • demonstrate administration of bacilli to an animal to reproduce the same morbid condition
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3
Q

antibacterials (3)

A
  • antibiotics
  • disinfectant
  • antiseptic
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4
Q

antibiotics administration

A
  • inside and outside the body
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5
Q

antibiotics (2)

A
  • natural, synthetic or semi-synthetic compound
  • can kill or inhibit growth of bacteria
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6
Q

what do antibiotics target (3)

A
  • cell wall synthesis
  • protein synthesis
  • DNA synthesis
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7
Q

disinfectants (2)

A
  • toxic
  • only be used to kill microbes on inanimate objects
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8
Q

antiseptic (2)

A
  • less toxic
  • can be applied to living tissues (the skin)
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9
Q

antibacterial agent

A
  • agents that are used to prevent bacteria specifically, and not other types of microorganisms
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10
Q

antimicrobial agents (2)

A
  • agent that destroys, or prevents the growth of, microorganisms
  • includes bacteria, mold, and fungi
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11
Q

chemotherapeutic agents (2)

A
  • used to directly or indirectly inhibit the uncontrolled growth and proliferation of cancer cells
  • toxic
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12
Q

what is one of the first chemotherapeutic agents

A
  • salvarsan
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13
Q

salvarsan

A
  • used to treat syphilis, relapsing fever, and African Trypanosoma
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14
Q

chemotherapeutic agents (3)

A
  • salvarsan
  • arsenate
  • atoxyl (toxic)
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15
Q

chemotherapeutic compounds against Mtb (3)

A
  • para-amino salicylic acid
  • dapsone
  • sulfanilamide
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16
Q

chemotherapeutic compounds: mechanism of sulfonamides (2)

A
  • pteridine and p-aminobenzoic acid normally combine to form dihydropteroic acid
  • sulfonamides block this synthesis, which prevents nucleotide biosynthesis
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17
Q

what was the first antibiotic

A
  • penicillin
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18
Q

penicillin

A
  • fungus that can kill bacteria
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19
Q

antibiotic against tuberculosis

A
  • streptomycin was the first ever effective antibiotic against TB
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20
Q

what produces streptomycin

A
  • soil bacterium Streptomyces griseus
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21
Q

streptomyces (3)

A
  • common soil microbes
  • found to be a source of antibiotics, accounting for ~70% of antibiotics
  • can produce other chemotherapeutic compounds
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22
Q

microbe synthesis of chemotherapeutic compounds (2)

A
  • statins
  • immunosuppressants
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23
Q

what kind of antibiotic classes are there (2)

A
  • bactericidal
  • bacteriostatic
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24
Q

bactericidal antibiotics (2)

A
  • kill the bacteria
  • bacteria presence and growth is not present after antibiotic is removed
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25
Q

bacteriostatic antibiotics (2)

A
  • suppress the growth of bacteria, keeping them in the stationary phase of growth
  • bacteria presence and growth will continue if antibiotic is removed
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26
Q

what are some mechanisms that bactericidal agents function by (4)

A
  • inhibit bacterial cell wall synthesis or disrupt membrane function
  • inhibit synthesis of proteins by bacteria
  • inhibit synthesis of RNA by bacteria
  • interfere with bacterial DNA replication and transcription
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27
Q

what are mechanisms that bacteriostatic agents function by (2)

A
  • prevent bacteria growth and multiplication
  • inhibit synthesis of proteins by bacteria
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28
Q

what are some antibiotic activities that can be measured (2)

A
  • minimal inhibitory concentrations (MIC)
  • minimal bactericidal concentrations (MBC)
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29
Q

how can MIC and MBC be measured (2)

A
  • fluorescence measurements
  • CO2 production
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30
Q

minimal inhibitory concentrations (MIC)

A
  • minimal concentration of a drug that inhibits growth of bacteria
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31
Q

minimal bactericidal concentrations (MBC)

A
  • minimal concentrations of a drug that kills the bacteria
32
Q

what are methods/experiments to determine MIC and MBC (3)

A
  • serial dilutions
  • disk diffusion arrays
  • the E test
33
Q

measuring MIC/MBC: serial dilution procedure (4)

A

1 organism cultured
2. organism grown to standard density in broth
3. tubes with increasing drug concentrations inoculated with standard number of organisms
4. concentrations of MIC and MBC determined based on bacterial growth in the tubes

34
Q

measuring MIC/MBC: disc diffusion arrays

A
  • bacteria are allowed to grow on discs containing known amounts of antibiotics
35
Q

disc diffusion array: susceptible organisms results (2)

A
  • zone of inhibition is created where the antibiotic was placed
  • indicates affected bacterial growth due to the antibiotic
36
Q

disc diffusion array: resistant organisms results (2)

A
  • no zone of inhibition is created where antibiotic is placed
  • indicates that bacterial growth is not affected by the antibiotic
37
Q

what does the E test measure

A
  • method to measure MIC
38
Q

E test mechanism (3)

A
  1. bacterial grows on agar plate
  2. antibiotic strip is placed on plate, creating a zone of inhibition
  3. MIC is determined where the edge of the inhibition eclipse intersects with the side of the E-test strip
39
Q

pharmacodynamics (2)

A
  • the study of a drug’s molecular, biochemical, and physiologic effects or actions
  • can measure the effects of antibiotics on bacteria
40
Q

how can pharmacodynamics measure effects of antibiotics on bacteria

A
  • measure the amount of bacterial colonies present at increasing concentrations of the antibiotic
41
Q

what do antibiotics generally target (3)

A
  • cell wall synthesis
  • nucleic acid synthesis
  • protein synthesis
42
Q

what do antibiotics target in the cell wall (3)

A
  • beta lactams
  • vancomycin
  • cell membrane
43
Q

what do antibiotics target in nucleic acid synthesis (3)

A
  • folate synthesis
  • DNA gyrase
  • RNA polymerase
44
Q

what do antibiotics target in protein synthesis (2)

A
  • 50S subunit
  • 30S subunit
45
Q

what are some relevant classes of antibiotics (5)

A
  • beta-lactams
  • glycopeptides
  • aminoglycosides
  • tetracyclines
  • macrolides/lincosamides
46
Q

what are beta lactam antibiotics mechanism of action: general (2)

A
  • inhibit transpeptidation step in peptidoglycan synthesis
  • stimulate autolysins; lytic enzymes
47
Q

what do beta lactam antibiotics binds

A
  • bind penicillin-binding proteins
48
Q

resistance mechanisms against beta lactam antibiotics (4)

A
  • gram-negative outer membrane alterations
  • porin mutations
  • beta-lactamase
  • modify target (penicillin-binding proteins)
49
Q

beta lactam antibiotics: spectrum of activity (2)

A
  • gram-positive
  • gram-negative
50
Q

glycopeptide antibiotics: mechanism of action

A
  • inhibit transglycosylation and transpeptidation steps in peptidoglycan synthesis
51
Q

what do glycopeptide antibiotics bind to

A
  • D-Ala-D-Ala
52
Q

glycopeptide antibiotics: resistance mechanisms (2)

A
  • gram-negative outer membrane alterations
  • modify target (substitute D-Ala-D-Ala with D-Ala-D-lactate)
53
Q

glycopeptide antibiotics: spectrum of activity

A
  • most effective against gram-positive bacteria
54
Q

aminoglycosides antibiotics: mechanism of action

A
  • bind 16S rRNA in 30S subunit of bacterial ribosome
55
Q

aminoglycosides antibiotics: resistance mechanisms (2)

A
  • inactivation of antibiotic by adding groups
  • mutation in 16S rRNA genes
56
Q

aminoglycosides antibiotics: spectrum of activity

A
  • broadly bactericidal
57
Q

tetracyclines antibiotics: mechanism of action

A
  • bind 16S rRNA in 30S subunit of bacterial ribosome
58
Q

tetracyclines antibiotics: resistance mechanisms (4)

A
  • inactivation of antibiotic
  • ribosome protection
  • mutation in 16S rRNA genes
  • efflux
59
Q

tetracyclines antibiotics: spectrum of activity

A
  • broadly bacteriostatic
60
Q

macrolides antibiotics: mechanism of action

A
  • bind 23S rRNA in 50S subunit of bacterial ribosome
61
Q

macrolides antibiotics: resistance mechanisms (3)

A
  • methylation of target
  • mutation in 23S rRNA genes
  • efflux
62
Q

macrolides antibiotics: spectrum of activity (2)

A
  • bacteriostatic mostly
  • bactericidal for some gram-positive bacteria
63
Q

bacterial growth and peptidoglycan

A
  • during growth, PG is constantly being hydrolyzed and cross-linked
64
Q

PG precursors

A
  • d-Ala d-Ala
65
Q

what are the proteins involved in PG formation

A
  • penicillin-binding proteins (Pbp)
66
Q

penicillin-binding proteins (3)

A
  • transglycosylases
  • transpeptidases
  • autolysins
67
Q

beta-lactam antibiotics mechanism of action: specifics (4)

A
  • beta-lactam antibiotics resemble PG precursors
  • PG crosslinking is inhibited as transpeptidase binds beta-lactam antibiotic instead of PG precursor
  • prevents binding to peptide chain building blocks
  • eventually leads to bacterial death (cells grow, but membrane doesn’t)
68
Q

beta-lactam antibiotics: structure (2)

A
  • all have beta-lactam ring, which defines their core activity
  • differ by R group, which determines specificity and binding
69
Q

vancomycin administration

A
  • intravenous
70
Q

what is vancomycin used to treat (5)

A
  • septicemia
  • infective endocarditis
  • skin and skin structure infections
  • bone infections
  • lower respiratory tract infections
71
Q

vancomycin function (2)

A
  • inhibition of cell-wall biosynthesis
  • similar to cationic antimicrobial peptides
72
Q

vancomycin target

A
  • gram positive bacteria
73
Q

what stage do beta-lactams block in PG synthesis

A
  • transpeptidation
74
Q

what stage does vancomycin block in PG synthesis (2)

A
  • transglycosylation
  • blocks the stage before transpeptidation
75
Q

why have fewer antibiotics been developed recently (2)

A
  • takes 10-15 years to develop
  • extremely costly
76
Q

what are the phases of antibiotic development (4)

A
  • screening
  • modification of lead compound
  • phase I through III clinical trials
  • market release

micb 308 (22 decks)

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