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Micro Quiz 1 > antibiotics > Flashcards

antibiotics Flashcards

1
Q

what is MIC?

A

minimum inhibitory concentration

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2
Q

what is MBC?

A

minimum bactericidal concentration

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3
Q

what methods are used to determine for selection of effective antibiotics? (list)

A

1: MIC and MBC - MIC
2: tube dilution method - MIC
3: Disc Diffusion (Kirby-Bauer)
4: beta-lactamase production

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4
Q

what does MIC and MBC-MIC tell you about a bacterium? how would you determine MIC?

A

allows for selection of effective antibiotics
clinical lab report that an infecting agent is sensitive or resistant to an agent takes MIC into account - determine it by tube dilution method (but tedious and can only be used with one antibacterial agent at a time)

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5
Q

what is the tube-dilution method? what can it tell you?

A

series of tube dilutions of the antibiotic in culture medium inoculated with purified infectious agent - see what the smallest amount needed to kill the bacteria is

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6
Q

how would you determine MBC?

A

aliquots are plated onto agar subsequent to culture tube growth

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7
Q

what is disc diffusion (kirby-bauer)?

A

method that provides multiple, simultaneous testing
agar plate is spread with inoculum of purified infectious agent
filter paper discs with various concentrations of antibiotic placed on surface
measure circular zones of inhibition of growth around each disc

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8
Q

what is the advantage of the disc diffusion method? the disadvantage?

A

multiple antibiotics can be tested all at once

cannot determine MBC

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9
Q

how is beta-lactamase production tested for?

A

rapid test based on chromogenic beta-lactam substrate changing color within a short incubation time after addition of a suspension of the infetious agent
nitrocefin commonly used as the agent
determines whether beta-lactam antibiotics will work

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10
Q

what are the four properties that ideal antibiotics should have?

A

1: drug should kill or inhibit one or more species of bacterium with no toxicity to host cells (including allergic reactions)
2: drug should not be destroyed or eliminated by the host before invading bacteria can be killed or inhibited
3: drug should not have lost its effectiveness because bacteria have become resistant to its action
4: drug should reach the sites that contain bacteria

no such ideal antibiotics exist yet

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11
Q

what are the seven major classes of antibiotics/antimicrobial compounds? (list)

A

1: antimetabolites (sulfonamides)
2: inhibitors of cell wall synthesis (beta-lactams and glycopeptides)
3: agens that alter membrane permeability (polymyxins and polyene)
4: inhibitors of protein synthesis (aminoglysides, macrolides, tetracycline, chloramphenicol)
5: inhibitors of nucleic acid synthesis (quinolone derivatives and rifampin)
6: miscellaneous antibiotics
7: antifungal drugs

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12
Q

what do antimetabolites do?

A

interfere with the synthesis or function of a substance involved in normal cell metabolism
often structurally similar to the natural substance

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13
Q

what are sulfonamides?

A

antimetabolites

antibacterial agents with structures similar to PABA

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14
Q

what is sulfanilamide?

A

member of sulfonamide group of antibiotics

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15
Q

how do sulfonamides work?

A

penetrate sensitive bacteria and inhibit production of folic acid by competitively inhibiting one of the enzymatic steps required for its synthesis

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16
Q

what if folic acid necessary for?

A

bacterial DNA synthesis

if no DNA made, bacteria stop dividing

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17
Q

what happens if sulfonamides are removed (ie after an initial treatment)?

A

actions are reversible so bacteria resume growth when drug removed

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18
Q

what does it mean for a drug to be bacteriostatic?

A

will halt bacterial growth but is reversible so that when drug is removed, bacteria will stop growing

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19
Q

what does it mean for a drug to be bactericidal?

A

the drug is not reversible and will completely stop bacterial growth permanently

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20
Q

what kinds of organisms can sulfonamides act against?

A

a wide range of bacteria and some protozoa

good for UTIs

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21
Q

what does dihydrofolate reductase do?

A

bacterial enzyme that reduces dihydrofolate to tetrahydrofolate

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22
Q

what does trimethoprim do?

A

inhibits dihydrofolate reductase

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23
Q

what can trimethoprim be used in conjunction with?

A

with sulfonamides - results in synergistic action

commonly used in conjunction to treat UTI

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24
Q

what does bactrim consist of?

A

trimthoprim and sulfamethoxazole - combination of a sulfonamide and a trimethoprim

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25
Q

what bacterial infection is isoniazid used to treat?

A

M. tuberculosis

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26
Q

how does isoniazid work?

A

interferes with synthesis of mycolic acid
converted to active form inside cell
this active form inhibits the enzyme InhA - essential for fatty acid elongation

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27
Q

what is mycolic acid?

A

organic material unique to the cell walls of mycobacteria (TB) and a small number of other types of bacteria

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28
Q

what is InhA?

A

enzyme that’s essential for FA elongation in mycobacteria particularly
isoniazid acts on it

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29
Q

what happens if isoniazid treatement is stopped?

A

bacteriacidal, so not reversible

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30
Q

where can isoniazid access bacteria?

A

penetrates well through the cytoplasmic membrane of human cells
important because TB is usually intracellular

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31
Q

which drugs are antimetabolites? (list)

A

1: sulfonamides
2: trimethoprim
3: isoniazid

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32
Q

which drugs are inhibitors of cell wall synthesis (list)?

A

1: penicillin
2: cephalosporins
3: beta-lactam rings but not otherwise similar to penicillin
4: beta-lactamase inhibitors
5: glycopeptides
6: cycloserine
7: bacitracin

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33
Q

what is the major toxic effect of penicillin?

A

rare but sometimes serious allergic reaction

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34
Q

why is penicillin specific for bacterial cells?

A

animal cells don’t have a cell wall, whereas the bacterial cells require the cell wall for multiplication

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35
Q

how many divisions must bacterial cells undergo before they can be killed by penicillin?

A

1-2 division is sufficient

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36
Q

how could you prevent the lethal action of penicillin?

A

growth is necessary for penicillin to be effective
so if you stop growth, ie by depriving the cells of a nutrient that’s necessary for growth, the penicillin won’t kill the cells

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37
Q

how does penicillin kill cells?

A

inhibit peptidoglycan synthesis
this inhibition is thought to uncouple control of endogenous degradative activities which normally ar synchronized with cell wall synthesis => cell lysis in hypotonic media

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38
Q

how are penicillins hydrolyzed?

A

penicillin G by stomach acid
4-membered lactam ring - since the ring is strained, it’s easily hydrolyzed

can also be hydrolyzed by bacterial enzymes (penicillinases)

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39
Q

what is penicillinase?

A

bacterial enzyme that will hydrolyze the beta-lactam ring on penicillin to activate it

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40
Q

what is the mechanism by which penicillin acts?

A

structural analog of peptidoglycan pentapeptide - bind and inactivate penicillin-binding proteins (PBPs)
major bacteriocidal action is inactivating the transpeptidase responsible for crosslinking

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41
Q

which penicillins are sensitive to acid hydrolysis?

A

G

not V or ampicillin

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42
Q

which penicillins are sensitive to penicillinase

A

G, V, and ampicillin

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43
Q

what are penicillin-binding proteins (PBPs)?

A

transpeptidases that are responsible for the terminal stages of peptidoglycan synthesis and reshaping the cell wall during growth and division

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44
Q

for what types of bacteria would you use penicillin G and V?

A

sensitive to acid hydrolysis and penicillinase but still drug of choice for many gram-positive, sensitive cocci
also some gram-negative cocci

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45
Q

what are the shortcomings of penicillin G?

A

acid lability - so no oral formulation
penicillinase sensitivity
development of allergic response
ineffective vs. G- enterics

use semisynthetic penicillins to get around all drawbacks except for the allergic reaction

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46
Q

what is the difference between penicillin G and V?

A

V is relatively acid stable, whereas penicillin G is not

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47
Q

which penicillins are not sensitive to penicillinase?

A

methicillin

oxacillin

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48
Q

what would you use ampicillin and amoxicillin to treat?

A

G- enteric bacilli

G+ bacilli

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49
Q

what is the advantage of ampicillin and amoxicillin over penicillin G and V?

A

treats broader spectrum
also can act on G- enteric bacilli
acid stable

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50
Q

what is the difference between ampicillin and amoxicillin?

A

amoxicillin has higher serum levels

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51
Q

what types of bacteria are tricarcillin and piperacillin active against?

A

against a wide variety of G-

not as effective against G+

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52
Q

what is the difference between tricarcillin and piperacillin?

A

tricarcilllin is a beta-lactam effective against pseudomonas aeruginosa - carbocypenicillin

piperacillin is most active against G- enteric bacilli including P. aeruginosa and anerobes (so can do what tricarcillin can) - ureidopenicillin

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53
Q

what types of bacteria would you use methicillin and oxacillin against?

A

against G+, though has slightly lower activity than other drugs
not useful against G-

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54
Q

what is MRSA?

A

methicillin resistant staphylococcus aureus

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55
Q

what is methicillin used for?

A

not used often anymore because of high incidence of interstital nephritis

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56
Q

what is the difference between methicillin and oxacillin?

A

oxacillin is a newer, more potent derivative
it’s acid resistant and available orally

methicillin is acid labile

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57
Q

how do cephalosporins compare to penicillins? when would you use cephalosporins over penicillin?

A

similar in mechanism of action
have 4-membered beta-lactam ring but substitute a dihydrothiazine ring instead of the thiazolidine ring in penicillins

both bacteriocidal

but ceph have greater acid stability - resistant to some penicillinases

used when patients are allergic to penicillin

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58
Q

against what bacteria are cephalosporins effective?

A

G+ and some G-

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59
Q

what are advantages of newer versions of cephalosporins?

A

active against pseudomonas

better penetration into CSF

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60
Q

what type of antibiotic is cefazolin? what is it active against?

A

first generation cephalosporin

active against G+ and against some G- but not P. aeruginosa

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61
Q

what type of antibiotic is cefuroxime? what is it active against?

A

second generation cephalosporin
more effective against G-
less effective against G+
not effective against P. aeruginosa

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62
Q

what type of antibiotics are ceftriaxone and ceftazidime? how are they improved over previous drugs of their type?

A

third generation cephalosporins

improved beta-lactamase stability and broader G- spectrum

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63
Q

what is ceftriaxone active against? what is the advantage of this drug?

A

G- particularly

has superior CNS penetration

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64
Q

what is ceftazidime active against?

A

effective against G- and P. aeruginosa

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65
Q

what type of antibiotic is aztreonam?

A

monobactam - has beta-lactam ring but otherwise not similar to penicillin

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66
Q

what type of antibiotic is imipenem?

A

carbapenem - has beta-lactam ring but otherwise not similar to penicillin

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67
Q

what types of bacteria would you use aztreonam against?

A

aerobic G-, including P. aeruginosa

inefficient against most G+

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68
Q

to which type of patients would you use aztreonam?

A

patients allergic to penicillins - won’t be allergic to this because it’s structurally dissimilar enough

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69
Q

how do azteronam and imipenem respond to beta-lactimases?

A

azteronam is resistant to most beta-lactamases

imipenem is resistant to most, but can be susceptible to those of MRSA and renal dipeptidase (so often given with a renal dipeptidase inhibitor)

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70
Q

what are the beta-lactimase inhibitors?

A

clavulanic acid
sulbactam
tazobactam

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71
Q

what is the purpose of beta-lactiase inhibitors?

A

no real antibiotic activity, but can extend the use of beta-lactam antibiotics

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72
Q

how is clavulanic acid used? what is it used for?

A

it’s a beta-lactamase inhibitor often used in combinations with amoxicillin - will extend the use of the amoxicillin by preventing the bacterial beta-lactimases from inactivating the penicillin

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73
Q

how is sulbactam used? what is it used for?

A

it’s a beta-lactamase inhibitor often used in combinations with ampicillin - will extend the use of the amoxicillin by preventing the bacterial beta-lactimases from inactivating the ampicillin

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74
Q

how do glycopeptides work as an antibacterial agent?

A

cell wall synthesis inhibitors

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75
Q

what are the glycopeptide antibiotics? (list)

A

vancomycin
teicoplanin
cycloserine
bacitracin

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76
Q

what type of antibiotic is vancomycin? what is it’s mechanism of action?

A

glycopeptide (complex, soluble)
binds to R-D-Ala-D-Ala structures => blocks peptidoglycan precursor transfer
may also permeabilize protoplasts, inhibit RNA synthesis

77
Q

when is vancomycin used? what are the disadvantages/side effects?

A

can be somewhat toxic, side effects on hearing via CN 8 and on kidneys
but used when less toxic antibiotics aren’t working
against serious systemic staphylococcal or enterococcal infections and clostridium difficile enterocolitis
only drug available for MRSA and multiply resistant enterococcus

78
Q

are there resistant strains to vancomycin?

A

yes:
vancomycin-resistant enterococcus faecalis (VREF) is a growing problem
vancomycin-resistant s. aureus (VRSA) recently identified

79
Q

what type of drug is cycloserine? what is it used for? what are its disadvantages?

A

glycopeptide antibiotic
secondary TB drug
toxic

80
Q

what is the mechanism of action of cycloserine?

A

it’s a D-alanine analog

inhibits L-alanine –> D-alanine and D-alanine + D-alanine –> D-alanine-D-alanine => inhibited cell wall syntheses

81
Q

what type of antibiotic is bacitracin? what is it used to treat?

A

glycopeptide

used for G+ organisms

82
Q

what is the mechanism of action of bacitracin?

A

inactivates phosphatase that regenerates the active form of the carrier lipid in murein precursor synthesis:
lipid PP –> lipid P + P

83
Q

when and how is bacitracin used? what is it often used in conjunction with?

A

toxic
restricted to topical therapy
in common antibiotic ointments such as neosporin
used in conjunction with polymyxin B and neomycin

84
Q

how do -cidal agents vary from b-lactams (in terms of requirements for activity)?

A

-cidal agents don’t require cell growth to kill the cells

85
Q

what are some -cidal agents?

A

polymyxin B

daptomycin (not underlined)

86
Q

against what bacteria is polymyxin B effective against?

A

G- enteric rods (especially important against pseudomonas)

87
Q

what is the mechanism of action of polymyxin B?

A

positively charged polypeptide
binds to negatively charged LPS in outer membrane
then binds to cytoplasmic membrane phospholipids
=> membrane leakage

88
Q

how is polymyxin B commonly used?

A

as topical agents

systemic use largely supplanted by more effective and less toxic agents

89
Q

what is the process of protein synthesis in bacteria?

A

1: mRNA binds to 30S
2: formylmethionyl tRNA and 50S subunit added => initiation complex
3: aminoacyl tRNA adds to ribosome
4: peptide bond is formed
5: translocation
6: chain extension
7: release of completed protein

90
Q

what type of antibiotic is streptomycin?

A

aminoglycoside

91
Q

when is streptomycin used?

A

no longer widely used except in TB and a few other special situations

92
Q

how was sterptomycin discovered?

A

in a search for antibiotics produced by soil bacteria

93
Q

what conditions is streptomycin inhibited?

A

positively charged at physiological pH

inhibited under anaerobic conditions or acid conditions (as in urine)

94
Q

what is required (from the bacteria) for streptomycin to be effective?

A

doesn’t enter cell readily so some metabolic activity by bacterium needed

95
Q

how does streptomycin compare with penicillin? (speed and final result to cell)

A

rapidly bacteriocidal

but not lytic (unlike penicillin)

96
Q

what is the mechanism by which streptomycin acts? how does the concentration alter action?

A

at low concentrations, only a few molecules get through
acts on 30S ribosomal subunit
distorts the acceptor site => misreading => bad proteins being made => membrane leakiness
this allows higher concentrations to enter the cell
at high concentrations, it inhibits the formation of the initiation complex and peptide bond formation

97
Q

are their resistant strains to streptomycin? if so, how do these occur?

A

yes, readily obtained, and resistant before treatment

selected for because it will kill off the bacteria that aren’t resistant

98
Q

what antibiotics are aminoglycosides? (list)

A 
streptomyocin
gentamicinin
tetracycline
doxycycline
erythromycin
azithromycin
chloramphenicol'
clindamycin
sreptogramins
oxazolidinones
mupirocin
99
Q

what type of antibacterial is gentamicin?

A

aminoglycoside

100
Q

how does gentamicin work?

A

inhibits 30S subunit

101
Q

what is the advantage of getamicin over streptomycin?

A

gentamycin acts on more than one protein on the 30S subunit, so it requires more than one mutation to develop resistance

102
Q

what are the downsides/side effects of aminoglycosides?

A

damage CN 8 (auditory, vestibular)

kidney damage

103
Q

when do you use aminoglycosides?

A

in serious infections where the antibiotic must be used in spite of the toxicity

104
Q

what types of antibacterials should you give to patients with compromised immune systems?

A

bacteriocidal ones rather than bacteriostatic ones

aminoglycosides and other “cidal” antibiotics are good for this

105
Q

what are the tetracycline antibiotics?

A

tetracycline
doxycycline
tigecycline

106
Q

how do tetracyclines work (ie mechanism of action)?

A

block the binding of the aminoacyl-RNA to 30S ribosomal subunit

107
Q

are tetracycline antibiotics bacteriostatic or bacteriocidal?

A

bacteriostatic

108
Q

what are the advantages of tetracyclines (in terms of practicality for treatment)?

A

well absorbed orally so good for out-patient treatment when therapy is needed over a week or two

109
Q

what bacteria are tetracyclines effective against?

A

have a broad spectrum of action - includes mycoplasma, rickettsia, chlamydia

110
Q

what are the side effects of tetracyclines?

A

teratogen (not safe for fetuses)
can give children under age 8 mottled enamel on their teeth (not serious side effect)
since it has such a broad spectrum of action, it can change the flora in the GI tract if given over a long period of time => diarrhea

111
Q

what type of antibiotic is tigecycline?

A

tetracycline

112
Q

what is the advantage of tigecycline over other tetracyclines?

A

most potent
has chemical side-chain that makes it refractory to a common mechanism of tetracycline resistance that involves an efflux pump

113
Q

what are the inhibitors of the 50S ribosomal function?

A 
erythromycin
azithromycin
chloramphenicol
clindamycin
sreptogramins
114
Q

how does erythromycin work?

A

blocks chain elongation

115
Q

what is erythromycin used to treat?

A

treats very wide spectrum of infections, similar to penicillin G
includes mycoplasma and chlamydia

116
Q

what type of drug is azithromycin?

A

type of 50S ribosomal function inhibitor

117
Q

what is the advantage of azithromycin over erythromycin?

A

higher activity and slightly broader spectrum

high and sustained tissue concentrations that increase at site of infection - due to phagocytes that migrate to the site

118
Q

how does chloramphenicol work?

A

blocks polypeptide chain elongation by inhibiting 50S subunit

119
Q

are the inhibitors of 50S ribosomal function bacteriocidal or bacteriostatic?

A

all bacteriostatic

120
Q

what are the side effects of chloramphenicol?

A

can rarely induce uncommon but sometimes lethal aplastic anemia
therefore not widely used

121
Q

when is chloramphenicol used?

A

infections in which it is vital for theraby

useful against some anaerobes, esp bowel ones like B fragiis

122
Q

what is clindamycin used against?

A

G+

moderate activity against anaerobes

123
Q

how does clindamycin work?

A

50S ribosomal function inhibitor

by inhibiting peptidyl transfer

124
Q

how does sreptogramins work?

A

binds 50S subunit

125
Q

what is the clinical prototyple of sreptogramins?

A

combination of dalfopristin and quinupristin (called synergin)
combination is 16-fold more active than either alone

126
Q

what is synergin used to treat?

A

MRSA
VREF
other multiply resistant bacteria

127
Q

how do oxazolidinones work?

A

inhibit translation by interaction with the ribosome
probably inhibit tRNA translocation
interacts with the 16S RNA and 23S rRNA of the 30S and 50S subunits

128
Q

what are oxazolidinones used against?

A

G+

potentially for VREF, MRSA, VRSA, other multiply resistant bacteria

129
Q

what is linezolid? what’s its trade name?

A

prototype of oxazolidinone

trade name = zyvox

130
Q

are oxazolidinones bacteriostatic or cidal?

A

bacteriostatic

131
Q

what are the advantages of oxazolidinones (in terms of treatment methods and side effects)?

A

can be applied by both oral and IV routes

don’t need to dose adjust for patients with renal impairment

132
Q

what is the mechanism of mupirocin action?

A

binds a specific tRNA syntethase (isoleucyl-tRNA synthetase) => prevents its function => no charged Ile-tRNAs for protein synthesis

133
Q

is mupirocin bacteriostatic or bacteriocidal?

A

bacteriostatic at low concentrations

if applied topically in high concentrations can be bacteriocidal

134
Q

what is mupirocin used to treat?

A

MRSA, esp. nasal carrier state
topical treatment of impetigo due to S. aureus or S. pyogenes
has weaker effects against natural surface flora

135
Q

what are the most common quinolones used?

A

floroquinolones (not underlined)
ciprofloxacin
moxifloxacin

136
Q

what are quinolones used to treat? (types of bacteria and types of infection)

A

some G+ cocci
enteric G- bacilli
P. aeruginosa

variety of infections including UTI, respiratory and anaerobic

137
Q

what is ciprofloxacin used to treat?

A

anthrax

also used as prophylactic when exposure to p anthracis is a risk (first responders)

138
Q

how do quinolones work?

A

inhibits enzyme DNA gyrase - needed for DNA synthesis

139
Q

are quinolones bacteriocidal or bacteriostatic?

A

bacteriocidal

140
Q

is there resistance to quinolones?

A

yes - emerging rapidly

esp to MRSA

141
Q

which patients should not receive quinolone treatment?

A

pregnant women

children (can damage growing bone)

142
Q

what type of drug is metronidazole? how does it work?

A

nitroimidazole

inhibits DNA replication - binds DNA and fragments it

143
Q

what kinds of bacteria is metronidazole used against?

A

anaerobic bacteria, especially bacteriodes species

certain protozoal infections (trichomoniasis and amebiasis)

144
Q

is metronidazole bacteriocidal or bacteriostatic?

A

bactericidal

145
Q

what conditions does metronidazole require? why?

A

anaerobic conditions

antibiotic must be reduced and activated by an electron transport protein (ferredoxin)

146
Q

what type of drug is rifampin?

A

inhibitor of RNA synthesis

147
Q

how does rifampin work?

A

inhibits transcription by binding to the b subunit of bacterial RNA polymerase
inhibits specific binding to DNA

148
Q

is rifampin bacteriocidal or bacteriostatic?

A

bacteriocidal

149
Q

is rifampin used in combination with other drugs? why or why not?

A

yes, often used in combination with other antibiotics because resistance develops rapidly if used alone

150
Q

what types of bacteria is rifampin used to treat?

A

secreted in saliva so useful as prophylactic against bacteria that enter via the nasopharyngeal route (so can prevent spread against N. menigitidis)

in combination with isoniazid or pyrazinamide against TB

151
Q

what is ethambutol used to treat? what is its mechanism of action? is it bacteriostatic or cidal?

A

TB
mechanism unknown
static against tubercle bacilli

152
Q

what is pyrazinamide used to treat? what is the mechanism of action? what is required for it to work?

A

against TB
mechanism unknown
requires activity of mycobacteria amidase to be activated

153
Q

what are the possible consequences of mixing antibiotics? (list)

A

1: indifference (additive)
2: synergistic
3: antagonistic

154
Q

what would be an example of potential antagonism (when mixing two antibiotics)?

A

giving penicillin, which requires growth, with a bacteriostatic agent (such as tetracycline)

155
Q

what would be an example of potential synergism (when mixing two antibiotics)?

A

giving an agent that damages the cell wall/membrane (such as penicillin) with an agent that is cidal but taken up poorly by bacterium

156
Q

when should you use more than one antibiotic? (5 reasons)

A

1: when synergism can be expected
2: when the susceptibility pattern of the most probably pathogens require use of more than one agent
3: when the likelihood of development of bacterial resistance is reduced
4: when the dosage of a toxic drug can be reduced
5: for a polymicrobial infection that requires the use of more than one agent

157
Q

what are the disadvantages of giving more than one antibiotic?

A

increased risk of side effects and superinfections
possible drug antagonism
increased cost

158
Q

what are the general reasons for antibiotic inactivity (mechanisms of resistance)?

A

1: antibiotic is inactivated, either extracellularly, intracellularly or both
2: antibiotic can’t enter cell or is actively pumped out
3: bacterial cell contains an altered enzyme that resists action of antibiotic
4: antibiotic can enter the cell but the drug-binding target site is replaced

159
Q

how can erythromycin be inactivated by bacteria?

A

with the enzyme erythromycin esterase - hydrolyzes the lactose ring

160
Q

how can chloramphenicol be inactivated by bacteria?

A

chloramphenicol acetyltransferase can acetylate it

161
Q

how can aminoglycoside antibiotics be inactivated by bacteria?

A

by aminoglycoside modifying enzymes - generally modifies drug during transport across the cytoplasmic membrane

162
Q

how can beta-lactam drugs be inactivated by bacteria?

A

beta-lactamases cleave the beta-lactam ring

163
Q

how can bacteria prevent entry of antibiotic into the cell? which antibiotics will this affect?

A

can alter membrane permeability by decreasing expression of outer membrane porins
will affect beta-lactams, nalidixic acid, chloramphenicol

inner membrane transporters can be altered
will affect amino glycosides - but rarely happens since usually deleterious

164
Q

which antibiotics can be effluxed from the cell?

A

tetracycline

fluconazole

165
Q

how can alteration of ribosomal targets provide antibiotic resistance? which drugs would this affect?

A

methylation of the 23S rRNA (component of the 50S subunit) - prevents erythromycin

alter the S12 of 30S subunit - gives streptomycin resistance

166
Q

how can alteration of cell wall precursor targets provide antibiotic resistance? which drugs would this affect?

A

gene changes to make enzyme that can make D-ala-D-lactate instead of D-ala-D-ala ligases
vancomycin and teichoplanin then can’t recognize D-ala-D-lactate

167
Q

how can alteration of target enzymes provide antibiotic resistance? which antibiotics would the affect?

A

altered PBPs => lower affinity or change in amount - methicillin resistance is associated with altered affinity PBPs

altered dihydropteroate synthetase => sulfonamide resistance

altered DHFR => trimethoprim resistance?

168
Q

what are the types of antifungal drugs?

A

1: affect membrane permeability
- amphotericin B
- nystatin
2: inhibitors of cell membrane synthesis
- azoles (systemic)
- fluconazole
- ketoconazole
3: inhibitors of cell wall synthesis
- caspofungin
4: antimetabolites
- flucytosine

169
Q

which drugs affect fungal membrane permeability?

A

amphotericin B
nystatin

both polyene compounds

170
Q

how do polyene compounds work?

A

bind to sterols in cell membranes

171
Q

why are polyene compounds selective for fungi?

A

bind better to the principle sterol in fungal cell walls = ergosterol
than the principal sterol in animal cell walls = cholesterol

172
Q

how is amphotericin B used (applied)? what does it do?

A

poorly absorbed in the GI tract
used systemically but toxic

destroys membrane integrity

173
Q

how is nystatin used (applied)?

A

too toxic for systemic use
used topically for oral fungal infections using the swish and swallow technique - can be done since not absorbed by GI tract well so can’t attain systemic access

174
Q

are polyene compounds fungicidal or fungistatic?

A

amphotericin B = fungicidal

nystatin = fungistatic except at high doses that are not physiologically attainable

175
Q

what are the inhibitors of fungal cell membrane synthesis?

A

azoles (systemic)
fluconazole
ketoconazole

176
Q

what are azoles used to treat?

A

oral candidiasis (thrush) and other systemic mycoses

177
Q

what types of patients need azoles?

A

ones with impaired immune systems, such as AIDS patients, who may require chronic suppression of recurrent fungal infections

178
Q

how are fluconazole and ketoconazole applied?

A

orally

179
Q

what are potential side effects of azoles?

A

hepatotoxicity occurs in 0.001% of patients

180
Q

how do azoles work?

A

inhibits ergosterol synthesis via inhibition of cytochrome P450 14a-demethylase => disturbed membrane and cell properties
inhibits hyphae synthesis => fungi more easily phagocytosed by PMNs and macrophages

181
Q

are azoles fungistatic or fungicitic?

A

fungistatic

182
Q

what are echinocandins? how do they work?

A

antifungal drugs that inhibit cell wall synthesis

inhibit glucan synthesis by inhibiting activity of 1,3-b-D-glucan synthase

183
Q

what are the two echinocandins?

A

caspofungin

anidulafungin (not underlined)

184
Q

are echinoandins fungicidal or fungistatic?

A

fungicidal

185
Q

what type of drug is flucytosine?

A

antimetabolite

186
Q

how does flucytosine work?

A

inhibits fungal protein synthesis by replacing uracil with 5-flurouracil in fungal RNA

also inhibits thymidylate synthetase via 5-fluorodeoxy-ruidine monophosphate => interferes with fungal DNA synthesis

187
Q

is flucytosine fungicidal or fungistatic?

A

can be either

depends on fungal isolate

188
Q

how do fungi develop resistance to drugs?

A

generally not understood, but seems to be in fungal genome - so no acquired resistance mechanisms have been discovered so far

common mechanism = increased expression of efflux pumps and alteration in targets of drugs

Micro Quiz 1 (9 decks)

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