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Veterinary Microbiology > Antimicrobial Chemotherapy > Flashcards

Antimicrobial Chemotherapy Flashcards

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Biology 101 flashcards
1
Q

what are chemotherapeutic agents?

A

chemical agents used to treat disease

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2
Q

who do chemotherapeutic agents do? (2)

A
  1. detstroy pathogenic microbes or

2. inhibit their growth within a host

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3
Q

what kind are most chemotherapeutic agents?

A

antibiotics

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4
Q

describe antibiotics

A

microbial products or their derivatives that kill susceptible microbes or inhibit their growth

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5
Q

what kind of disease was there lots of in the 1500’s?

A

venereal

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6
Q

what were the only 2 treatment options for venereal and other diseases in the 1500’s/early medicine?

A
  1. mercury agents or paste

2. arsenic

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7
Q

describe the link between STDs and malaria in early medicine

A

patients with STDs AND malaria had a fever that killed that the siphylis, so doctors tried heat chambers to recreate or straight injected patients with malaria

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8
Q

who accidentally discovered penicillin in 1928? how?

A

Alexander Fleming; observed penicillin activity on a contaminated plate

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9
Q

did Fleming think penicillin could go further? who helped?

A

he did not; Florey, Chain, and Heatly demonstrated effectiveness

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10
Q

what is selective toxicity?

A

the ability of a drug to kill or inhibit pathogen while damaging the host as little as possible; a general characteristic of antimicrobial drugs

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11
Q

what is therapeutic dose?

A

drug level required for clinical treatment; a general characteristic of antimicrobial drugs

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12
Q

what is toxic dose?

A

the drug level at which the drug becomes too toxic for the patient and produces side effects

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13
Q

what is the therapeutic index?

A

the ratio of toxic dose to therapeutic dose

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14
Q

do you want a low or high therapeutic index? why?

A

you want a higher therapeutic index because it will have better/higher selective toxicity

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15
Q

what are side effects?

A

undesirable effects of drugs on host cells

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16
Q

what are narrow-spectrum drugs?

A

attack only a few different pathogens; a general characteristic of antimicrobial drugs

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17
Q

what are broad spectrum drugs?

A

attack many different kinds of bacteria; a general characteristic of antimicrobial drugs

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18
Q

what is a cidal agent?

A

kills the target pathogen

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19
Q

what is a static agent?

A

reversibly inhibits growth of microbes

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20
Q

what 3 things have an effect of the effectiveness of antimicrobial drugs?

A
  1. concentration
  2. microbe
  3. host
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21
Q

how is antimicrobial drug effectiveness expressed? (2 ways)

A
  1. MIC: minimal inhibitory concentration: the lowest concentration of the drug that PREVENTS GROWTH of the pathogen
  2. MLC: minimal lethal concentration: the lowest concentration of a drug that KILLS PATHOGENS
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22
Q

what are the 4 main modes of action of antimicrobial drugs?

A
  1. inhibitors of cell wall synthetis
  2. protein synthesis inhibitors
  3. metabolic antagonists
  4. nucleic acid synthesis inhibition
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23
Q

name 3 antibiotic drugs whose mode of action is inhibiton of cell wall synthesis

A
  1. penicllins
  2. cephalosporins
  3. vancomycin
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24
Q

what is the most crucial structural feature of penicillins?

A

the B-lactam ring

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25
Q

what does the B-lactam ring of penicillins do?

A

is essential for bioactivity

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26
Q

what do many penicillin resistant organisms produce and what does it do?

A

B-lactamase (also called penicillinase), which hydrolyzes a bond in this the B-lactam ring, limiting efficacy of penicillins

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27
Q

describe the specific cell wall synthesis-inhibiting mdoe of action of penicillins

A

blocks the enzyme that catalyzes transpeptidization, preventing synthesis of complete cell walls leading to lysis of cell

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28
Q

what is transpeptidization?

A

formation of cross-links in peptidoglycan

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29
Q

what type of bacteria are the target of penicillins?

A

growing bacteria that are synthesizing new peptidoglycan

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30
Q

what are the 2 types of naturally-occurring penicllins? are they broad or narrow-spectrum?

A

Penicillin V and G; narrow spectrum

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31
Q

why are semisynthetic penicillins broader spectrum than naturally occuring penicillins?

A

the bulkier side chains make them more difficult for B-lactamase enzymes to degrade

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32
Q

is resistance to penicillin a problem? for semisynthetics?

A

yes, and also for semisynthetics

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33
Q

compare the structure and function of cephalosporins to penicillins

A

structurally and functionally similar to penicillins

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34
Q

describe cephalosporins (target range and use)

A

broa spectrum antibiotics that can be used by most patients allergic to penicllin

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35
Q

how many categories of cephalosporins are there based on their spectrum of activity?

A

4

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36
Q

what kind of antibiotic is vancomycin (structureish)

A

glycopeptide antibiotic

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37
Q

describe the cell wall synthesis-inhibiting mode of action of vancomycin

A

prevents transpeptide from ever binding

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38
Q

what is vancomycin important for?

A

important for treatment of antibiotic-resistant staphylococcal and enterococcal infections

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39
Q

what was vancomycin previously considered and why is this a concern now?

A

was the drug of last resort when nothing else worked, so the rise in RESISTANCE to vancomycin is concerning, especially with the MERSA strains that are now resistant

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40
Q

would you expects inhibitors of cell wall synthesis ro work better against gram positive or gram negative bacteria? why?

A

work better against gram positive because those bacteria have only one layer of peptidoglycan that is not protected by an outer membrane like gram negative bacteria’s 2 layers of peptidoglycan are

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41
Q

do eukaryotic cells have peptidoglycan? what does this mean about the selective toxicity of cell wall inhibitor anytbiotics?

A

no; pretty high selective toxicity because can target bacteria without targeting us

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42
Q

name 3 antibiotics whose mode of action is protein synthesis inhibition

A
  1. aminoglycosides
  2. tetracyclines
  3. macrolides
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43
Q

where do protein synthesis-inhibiting antibiotics bind? how can they find/do this?

A

specifically to the bacterial ribosome, can differentiate due to the different ribosome densities between bacterial and eukaryotic ribosomes

44
Q

list the 4 different steps in protein synthesis that are targets of protein synthesis-inhibiting antibiotics

A
  1. amicoacetyl-tRNA binding
  2. peptide bond formation
  3. mRNA reading!
  4. translocation
45
Q

describe the specific protein synthesis-inhibiting mode of action of aminoglycosides

A

bind to 30S ribosomal subunit and interfere with protein synthesis by DIRECTLY inhibiting the process and by causing MISREADING of the mRNA

46
Q

what kind of target spectrum are aminoglycoside antibiotics?

A

broad spectrum

47
Q

describe the target spectrum of tetracycline antibiotics

A

broad spectrums

48
Q

/are tetracyclines bactericidal or bacteriostatic?

A

bacteriostatic

49
Q

describe the specific protein synthesis-inhibiting mode of action of tetracyclines

A

target the 30S subunit (like aminoglycosides) and slow down protein synthesis (static) and cause SOME misreading but not as much as aminoglycosides

50
Q

give an example of a macrolide

A

erythromycin

51
Q

describe the macrolide erythromycin (spectrum range and static or cidal)

A

broad spectrum, bacteriostatic

52
Q

describe the specific protein synthesis-inhibiting mode of action of the macrolide erythromycin

A

binds to 50S!! subunit to inhibit bacterial protein elongation

53
Q

when are macrolides used?

A

for patients who are allergic to penicillin

54
Q

describe metabolic antagonists?

A
  1. act as antimetabolites

2. are structural analogs

55
Q

how do metabolic antagonists act as antimetabolites?

A

antagonize or block functioning of metabolic pathways by competetively inhibiting the use of metabolites by key enzymes

56
Q

how are metabolic antagonists structural analogs?

A

they are molecules that are structurally similar to, and compete with, naturally occurring metabolic intermediates to block normal cellular metabolism

57
Q

list the 2 antimicrobials (and specify which one is an antibiotic) whose mode of action is metabolic antagonism

A
  1. sulfa drugs or sulfonamides

2. trimethroprim

58
Q

describe the structural analog nature of sulfa drugs/sulfonamides

A

structurally related to sulfanilamide, a PABA analog; PABA is used by many pathogens for the synthesis of folic acid

59
Q

how are sulfa drugs slecetively toxic?

A

due to competitive inhibition of folic acid synthesis enzymes

60
Q

describe trimethoprim

A

a synthetic antibiotic that also interferes with folic acid production

61
Q

what is the spectrum range of trimethoprim?

A

broad spectrum antibiotic

62
Q

how is trimethoprim often used?

A

often combined with sulfa drugs to increase efficacy of treatment

63
Q

what does the combination of sulfa drugs and trimethoprim do?

A

blocks to 2 steps in the folic acid pathway = more effective

64
Q

what are the most commonly used antibacterial drugs?

A

nucleic acid synthesis inhibitors

65
Q

describe nucleic acid synthesis inhibitors modes of action (2)

A
  1. inhibit DNA polymerase and topoisomerases (floroquinolones)
  2. inhibit RNA polymerase (rifamycins)
66
Q

are nucleic acid synthesis inhibitors as selectively toxic as other antibiotics? why or why not?

A

no, because bacteria and eukaryotes do not differ greatly in the way they synthesize nucleic acids

67
Q

describe the specific nucleic acid-inhibiting mode of action of fluoroquinolones

A

act by inhibitng bacterial DNA gyrase and topoisomerase II

68
Q

describe the spectrum range of fluoroquinolones

A

broad spectrum antiobiotics

69
Q

are fluoroquinolones bacteriostatic or bactericidal?

A

bactericidal

70
Q

what range of infections do flouoroquinolones treat?

A

a wide variety (duh bc they’re broad spectrum)

71
Q

what has antiviral drug development been slow?

A

because it is difficult to specifically target viral replication

72
Q

what has the success of antiviral drugs been in the past?

A

mixed

73
Q

what is the fate of a vast majority of viral infections?

A

cannot be cured

74
Q

what 2 main things do some antiviral drugs do to an illness? give example

A
  1. limit duration (flu)

2. limit severity (herpes, HIV)

75
Q

what do the current antiviral drugs in use do?

A

inhibit virus-specific enzymes and life cycle processes

76
Q

what type of antiviral agent is Tamiflu?

A

antiviral

77
Q

what is the mode of action of tamiflu?

A

neuriminidase inhibitor

78
Q

is Tamiflu a cure for influenza? what does it do?

A

not a cure, but shortens course of illness

79
Q

how many types of anti-HIV drugs are there?

A

5

80
Q

why are there so many kinds of anti-HIV drugs?

A

because it is so widespread and mutates so much

81
Q

name the 5 kinds of anti-HIV drugs

A
  1. nucleoside reverse-transcriptase inhibitors (NRTIs)
  2. nonnucleoside reverse-transcriptase inhibitors (NNRTIs)
  3. protease inhibitors (PIs)
  4. integrase inhibitors
  5. fusion inhibitors
82
Q

describe how nucleoside reverse-transcriptase inhibitors work

A

target and interfere with critical steps in viral replication processes

83
Q

describe how nonnucleoside reverse-transcriptase inhibitors work

A

prevent HIV DNA synthesis by selectively binding to and inhibiting the viral reverse transcriptase enzyme

84
Q

how do protease inhibitors work?

A

block the activity of the HIV protease needed for the production of all viral proteins

85
Q

how do integrase inhibitors work?

A

prevent the incorporation of the HIV genome into the host’s chromosome

86
Q

how do fusion inhibitors work?

A

prevent HIV entry into cells

87
Q

how are most HIV drugs given and why?

A

as cocktail mixes of multiple kinds of drugs to curtail resistance

88
Q

which 2 antimicrobials are most selectively toxic? in order

A
  1. anitbiotics

2. antivirals

89
Q

what 2 antimicrobial agents have the lowest therapeutic index and why?

A
  1. antiprotozoans
  2. antifungals
    bc those cells are similar to eukaryotic cells; hard to target without killing us too
90
Q

why are there fewer effective antifungal agents? (2)

A

because of the similarity of eukaryotic fungal cells to human and animal cells; most have low therapeutic index and are toxic

91
Q

what type of fungal infection is easier to treat?

A

superficial mycosis; easier than systemic mycoses

92
Q

what may be used to treat fungal infections?

A

a combination of drugs

93
Q

give an example of a superficial mycosis

A

candida

94
Q

what routes of antifungal mediciation is available to treat superficial mycoses? (2)

A
  1. topical

2. oral

95
Q

what is the mode of action of antifungal medications to treat superficial mycoses? (2)

A
  1. disrupts membrane permeability and inhibits sterol synthesis
  2. disrupts mitotic spindle, may inhibit protein and DNA synthesis
96
Q

describe systemic mycoses

A

difficult to control and can be fatal

97
Q

list the 3 common drugs used to treat systemic mycoses, the modes of actions of 2, and the use of the third

A
  1. Amphotericin B: binds sterols in membranes
  2. 5-flucytosine: disrupts RNA function
  3. Fluconazole: low side effects, used prophylactically
98
Q

is the mechanism of action for many anti-protozoan drugs currently known?

A

not precisely

99
Q

give 3 examples of antiprotozan drugs

A
  1. some antibiotics that inhibit bacterial protein synthesis
  2. quinines: anti-malarial, include chloroquine and mefloquine
  3. metronidazole: treats Entamoeba infections
100
Q

what are the 3 types of drug resistance?

A
  1. intrinsic
  2. acquired
  3. presistence (drug-tolerant bacteria)
101
Q

give an example of intrinic drug resistance by bacteria

A

mycoplasma resistance to B-lactam and other antibiotics because no cell wall

102
Q

describe acquired drug resistance

A

occurs when there is a change in the genome of a bacteria that converts it from one that is sensitive to an antibiotic to one that is resistant

103
Q

describe drug-tolerant bacteria

A

lack the mechanisms for antibiotic resistance, just ignore the presence of antibiotics

104
Q

where are drug-tolerant bacteria found?

A
  1. embedded in biofilms

2. bacteria growing too slowly to be inhibited

105
Q

what are the 4 mechanisms of drug resistance?

A
  1. modify the target of the antibiotic
  2. drug inactivation
  3. minimize the concentration of the antibiotic in the cell
  4. bypass the biochemical reaction inhibited by the agent or increase the production of the target metabolite
106
Q

what are the 3 methods to overcome drug resistance?

A
  1. give drug in appropriate concentrations to destroy susceptible microbes and most spontaneous mutants
  2. give 2 or mroe drugs at the same time
  3. use drugs only when absolutely necessary
107
Q

what are 2 possible future solutions to overcome drug resistance?

A
  1. continued development of new drugs

2. use of bacteriophages to treat bacterial disease

Veterinary Microbiology (11 decks)

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