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Bio 55 > Antimicrobial Drugs > Flashcards

Antimicrobial Drugs Flashcards

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1
Q

Define Chemotherapy

A

-Anything that requires chemicals (what she said)

-the use of drugs to treat a disease (slide definition)

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2
Q

Define antimicrobial drugs

A

-interfere with the growth of microbes within a host

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3
Q

Define antibiotic

A

A substance produced by a microbe that, in small amounts, inhibit another microbe

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4
Q

Define selective toxicity

A

-killing harmful microbes without damaging the host
(Which kills the microbe but not the host)

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5
Q

Define antimicrobial drugs

A

-synthetic substances that interfere with the growth of microbes

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6
Q

Who discovered penicillin?
What year?

A

-Alexander Fleming
-1928

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7
Q

What red dye was used for streptococcal infections ?

A

-Prontosil red dye

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8
Q

When were the first trials of penicillin?

A

1940

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9
Q

What is a growing problem today with antibiotics?

A

Antibiotic resistance

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10
Q

What does the term “magic bullet” mean ?

Who coined the term?

A

-kills microbes easy to make stable on shelf, safe to host

-Paul Erlich

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11
Q

Penicillin is produced by what mold?
Who discovered?
What year?

A

-Penicillium
-Alexander Fleming
-1928

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12
Q

Who performed the first clinical trials of penicillin?
What year?

A

-Howard Florey & Ernst Chain

-1940

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13
Q

Define Narrow spectrum of Antimicrobial activity

A

-drugs that affect a narrow range of microbial Types

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14
Q

Define Broad-spectrum antibiotics

A

-affect a broad range of gram-positive or gram-negative bacteria

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15
Q

Narrow spectrum antibiotics are used more for ?
-eukaryotes
-prokaryotes

A

-eukaryotes

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16
Q

Broad spectrum antibiotics are used more for?
-prokaryotes
-eukaryotes

A

-prokaryotes

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17
Q

What antibiotic (from the slides) has the broadest spectrum ?

A

Tetracycline

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18
Q

What 4 antimicrobial drugs are used for prokaryotes ?
(From the slide)

A

-isoniazid (mycobacteria)
-streptomycin (mycobacteria, gram -)
-penicillin (gram +)
-tetracycline (mycobacteria, gram -, gram +, chlamydia, rickettsia)

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19
Q

What 5 antimicrobial drugs are used for eukaryotes?
(From the slide)

A

-ketoconazole (fungi)
-mefloquine [malaria] (Protozoa)
-niclosamide (Helminthes)
-praziquantel (Helminthes)
-acyclovir (viruses)

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20
Q

Define bacteriocidal

A

Kills microbe directly

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21
Q

Define bacteriostatic

A

-prevents microbes from growing

(Along with immune system, can clear infection)

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22
Q

Define superinfection

A

Overgrowth of normal microbiota that is resistance to antibiotics

(Usually long term in the hospital )

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23
Q

What are the 5 major action modes of antimicrobial drugs?

A

-inhibition of cell wall synthesis
-inhibition of protein synthesis
-inhibition of nuclei acid
-injury to plasma membrane
-inhibition of metabolite synthesis

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24
Q

Explain inhibition of cell wall synthesis
(Antimicrobial drugs)

What drugs?

A

*affect cell wall

-Very selective to bacteria
-penicillins
-bacitracin
-vancomycin
-cephalosporins

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25
Q

Explain inhibition of protein synthesis
(Antimicrobial drugs)

What drugs?

A

*affect translation

-usually attack 70s ribosome in different places
-erythromycin,
-streptomycin
-chloramphenicol
-tetracyclines

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26
Q

Explain inhibition of nucleic acid replication & transcription
(Antimicrobial drugs)

A

*affect replication & transcription

-drugs that are virus specific usually
-quinolones
-rifampin

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27
Q

Explain injury to plasma membrane
(Antimicrobial drugs)

A

*affect plasma membrane

-very few can be used because host also has plasma membrane
-polymyxin B

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28
Q

Explain inhibition of essential metabolite synthesis
(Antimicrobial drugs)

A
  • affect enzyme

-sulfanimide trimethoprim

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29
Q

Is polymyxin b selectively toxic?

Explain?

A
  • it is not selectively toxic
    -polymyxin b affects plasma membrane of microbes but can also damage plasma membrane of host , hence NOT selectively toxic
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30
Q

What are some inhibitors of cell wall synthesis?

Which was the first one?

A

-penicillin (first one)
-natural penicillins (penicillin G, original penicillin)
-semisynthetic penicillins (tweaked for resistant forms)
-extended-spectrum penicillins (tweaked for resistant forms)

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31
Q

Explain how inhibitors of cell wall synthesis works.

A

-does not stop current grown cell wall, only PREVENTS new cell wall forming

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32
Q

Does penicillin affect previously formed cross links of cell wall? What about new cross links?

A

-previous cross links are not affected, but penicillin inhibits new cross links from being formed

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33
Q

What is the active ingredient that prevents cross linking of NAM units ? (In penicillin)

A
  • B-lactam ring
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34
Q

B-lactam ring?

A

Prevents the cross-linking of peptidoglycans, interfering with the cell wall construction (especially gram-positive)

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35
Q

How are natural penicillins made?

A

-extracted from Penicillium cultures

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36
Q

What 2 natural penicillins are there?
How are they taken ?

A

-penicillin G (injected)
-penicillin V (oral)

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37
Q

What is natural penicillin susceptible to ?

A

-penicillinases (B-lactamases)

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38
Q

How did penicillinase come to be?

A

Penicillinase evolved from certain microbes

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39
Q

Is natural penicillin broad or narrow spectrum?

A

Narrow

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40
Q

Explain semisynthetic penicillin.

A

Contain chemically added side chains, making them resistant to penicillinases

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41
Q

Penicillinases can affect which penicillin ?

-natural penicillin
-semisynthetic penicillin

A

-natural penicillin

Semisynthetic penicillin can resist penicillinases

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42
Q

Which penicillin requires injection ?

A

-penicillin G

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43
Q

Which penicillin can be taken orally ?

A

-penicillin V

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44
Q

Explain the concentration in blood of penicillin G (injection version)

A

-high initial concentration, but then drops quickly

(Highest concentration)

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45
Q

Explain the concentration in blood for penicillin g (oral version)

A

Not as high of concentration but last a little longer

(2nd highest concentration)

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46
Q

Explain the concentration in blood for procaine penicillin

A

Lower concentration, must be taken multiple time because of this.

(3rd highest concentration)

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47
Q

Explain the concentration in blood for Benzathine penicillin

A

-lowest concentration, last longest must be taken continuously

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48
Q

What are some penicillinase-resistant penicillins ?

A

-methicillin
-oxacillin

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49
Q

-What are some extended-spectrum penicillins
-what are they effective against ?

A

-aminopenicillins, ampicillin, amoxicillin

-effective against gram-negative and gram-positive

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50
Q

Explain penicillins plus B-lactamase inhibitors

A

-contain clavulanic acid, a non competitive inhibitor of penicillinase

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51
Q

explain Carbapenems

A

-substitute a C for an S and add a double bond to the penicillins nucleus

-Broad spectrum
-Primaxin, doripenem

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52
Q

Explain monobactum

A

-not used much because there’s better alternatives
-synthetic; single ring instead of the B-lactation double ring
-low toxicity; works against only CERTAIN gram-negatives
-aztreonam

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53
Q

What drug works similar to penicillin ?

A

Cephalosporins

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54
Q

Is the B-lactam ring similar or different than penicillin?

A

Different

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55
Q

Some polypeptide antibiotics?

A

-bacitracin (topical, works against gram +)

-vancomycin (keeps cell from secreting NAG, NAM)
*Glycopeptide
*Last line against antibiotic resistant MRSA

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56
Q

What antibiotic is considered a “last resort” for antibiotic resistant MRSA?

A

Vancomycin

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57
Q

2 antimycobacterial antibiotics?

A

-Isoniazid (INH)
*inhibits mycolic acid synthesis in mycobacteria
-Ethambutol
*inhibits incorporation of mycolic acid into the cell wall

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58
Q

Isoniazid and ethambutol will work for people who have ?

A

-tuberculosis
-leprosy

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59
Q

How does Inhibition of cell wall synthesis work?

A

-prevents bacteria from increasing the amount of peptidoglycan by interfering cross bridge formation

60
Q

Does cell wall synthesis inhibitors work on fully formed bacteria? Y/N

Explain

A

NO, it only inhibits new cross bridges from forming, does not affect previously formed cross bridges

61
Q

What phase does cell wall synthesis inhibitors affect?

A

Log phase of growth curve

62
Q

Do cell wall synthesis inhibitors affect plant or animal cells ?

Explain ..

A

-Does NOT affect either because neither have peptidoglycan

63
Q

What do protein synthesis inhibitors do?

Examples of some

A

-target bacterial 70s ribosomes

-chloramphenicol, erythromycin, streptomycin, tetracyclines

64
Q

*** KNOW THIS

What does chloramphenicol do ?

A

Binds to 50s portion and inhibits formation of peptide bond

65
Q

*** KNOW THIS

What does erythromycin do ?

A

Binds to the 23s rRNA molecule in the 50s subunit not allowing tRNA to attach

66
Q

*** KNOW THIS

What does tetracyclines do ?

A

Interfere with attachment of tRNA to mRNA-ribosome complex

67
Q

*** KNOW THIS

What does streptomycin do ?

A

Changes shape of 30s portion, causing code on mRNA to be read incorrectly

68
Q

Is chloramphenicol broad or narrow spectrum ?

A

-broad spectrum

69
Q

What does chloramphenicol do?

A

-inhibits peptide bond formation
-can suppress bone marrow and affect blood cell formation

70
Q

What antibiotic should NOT be given to children or pregnant women ?

Explain.

A

-Chloramphenicol

-suppresses bone marrow and affect blood cell formation

71
Q

What are antibiotics that should NOT be used during pregnancy?

A

-chloramphenicol
-streptomycin
-kanamycin
-tetracycline

-bactrim
-ciprofloxacin
-furadantin
-macrodantin
-macrobid
-minocyline
-Septra
-aminoglyosides
-

72
Q

Why can’t streptomycin, kanamycin & tetracycline be used during pregnancy ?

A

-They are teratogenic (agent causing malformation in embryo)

-Streptomycin & kanamycin can cause hearing loss

-tetracycline can lead to weakening hypoplasia and discoloration of long bones and teeth

73
Q

Characteristics of aminoglycosides

A

-amino sugars linked by glycoside bonds
-change the shape of the 30s subunit of the 70s ribosome
-can cause auditory damage (not recommended for pregnant)
-streptomycin, neomycin, gentamicin
-teratogenic. — harmful to a pregnancy

74
Q

Define teratogenic

A

-harmful to a pregnancy

75
Q

Characteristics of tetracyclines

A

-produced by streptomyces spp.
-interfere with the tRNA attachment to the ribosome
-broad spectrum penetrates tissues, making them valuable against rickettsias and chlamydias
-can suppress normal intestinal microbiota

76
Q

What is good against rickettsias and chlamydias?

A

Tetracyclines

77
Q

What can kill normal intenstinal microbiota ?

Should probiotics be taken with this ?

A

-tetracyclines

-since intestinal microbiota can be affected, probiotics SHOULD be taken with tetracyclines

78
Q

What are some protein synthesis inhibitors ?

A

-glycylcyclines
-macrolides

79
Q

Characteristics of glycylcyclines

A

-broad spectrum; bacteriostatic
-bind to the 30s ribosomal subunit
-inhibits rapid effluent; administered intravenously
-useful agains MRSA

80
Q

Characteristics of macrolides

A

-Contain a macrocyclic lactose ring
-narrow spectrum against gram-positives
*erythromycin

81
Q

Example of macrolide?

A

Erythromycin

82
Q

Describe erythromycin

A

“Large & spiky”

83
Q

Other antibiotics that inhibit proteins synthesis and attach to 50s or 30s subunits of ribosome

A

-streptogramins
-oxazolididnones
-pleuromutilins

84
Q

Stretpogramins attach to what ?

A

50s subunit

85
Q

Streptogramins work against gram _________ that are _______to other antibiotics

A

-positive

-resistant

86
Q

Oxazolidinones bind to ?

A

-50s/30s subunit interface

87
Q

Oxazolidinones helps combat ?

Is it natural or synthetic?

A

-MRSA
-synthetic

88
Q

Pleuromutilins are effective against what?

How is it administered ?

A

-gram positives

-topical

89
Q

What causes injury to the plasma membrane ?

A

-lipopeptides
-polymyxin B
-amphotericin B

90
Q

Inhibition of nucleic acid synthesis, what are the effects?

A

-interfere with DNA replication replication and transcription

-nucleoside analogs (used against viruses)
(Viruses dont have any proofreading, that’s how its used)

91
Q

Inhibition of synthesis of essential metabolites, what are the effects.

A

-anti-metabolites compete with normal substrates for an enzyme

*sulfanilamide competes with para-aminobenzoic acid (PABA), stopping the synthesis of folic acid.

*main metabolite pathway attacked is the pathway that makes folic acid.

*bacteria have to make own folic acid

92
Q

What are some nucleic acid inhibitors ?

A

-Rifamycin
-quinolone & fluoroquinolones

93
Q

What does rifamycin do ?

A

-inhibits mRNA synthesis
-penetrates tissues; antitubercular activity

94
Q

What do quinolone and fluoroquinolones do ?

A

-Nalidixic acid inhibits DNA gyrase , is synthetic

-norfloxacin and ciprofloxacin is broad spectrum, affects normal flora, so usually last choice

95
Q

Characteristics of sulfonamides

A

-inhibit the folic acid synthesis needed for nucleic acid and protein synthesis

-competitively bind to the enzyme for PABA production, a folic acid precursor

-combination of trimethoprim and sulfamethoxazole (TMP-SMZ) is an example of a drug synergism

96
Q

What are some anti fungal drugs that inhibit ergosterol synthesis?

A

-Polyenes
-S Amphotericin B
-azoles
-miconazole
-triazole
-allylamines
-for azole-resistant infections

97
Q

Example of anti fungal that affects fungal cell wall?

A

Echinocandins - inhibit synthesis of B-glucan

98
Q

Example of antifungal that inhibit nucleic acid

A

Flucytosine- cytosine analog interferes with RNA synthesis

99
Q

characteristics of griseofulvin

A

-produced by penicillium
-inhibits microtubule formation
-active against superficial dermatophytes

100
Q

What is tolnaftate used for ?

A

Athletes foot

101
Q

What does pentamidine do?

A

-anti pneumocystis; may bind to DNA

102
Q

What is the newest drug?

A

Antiviral drug

103
Q

What do antiviral drugs do ?

A

-Block receptors on host cell

-Block entry/exits from host cell

104
Q

Antiviral drugs are entry and fusion inhibitors , explain

A

-block the receptors on the host cell that bind to the virus

-block fusion of the virus and cell

105
Q

Antiviral drugs additional functions: uncoating, genome integration, and nucleic acid synthesis inhibitors. Further explain .

A

-prevent viral uncoating
-inhibit viral DNA integration into the host genome
-nucleoside analogs inhibit RNA or DNA synthesis

106
Q

Acyclovir is a treatment for what ?

A

Herpes

107
Q

What are usually good for RNA viruses?

A

Interferons

108
Q

What promotes interferon production ?

A

Imiquimod

109
Q

Explain interferons

A

-produced by viral-infected cells to inhibit further spread of the infection

110
Q

Antivirals for treating HIV/AIDS?

A

Antiretroviral
-nucleoside analog (zidovudine)
-nucleotide analog (tenofovir)
-non-nucleoside inhibitors (nevirapine)
-protease inhibitors (raltegravir)
-integrase inhibitors (miraviroc)
-fusion inhibitors (enfuvirtide)

Various combinations for each pt

111
Q

What are some anti protozoan drugs? (Mostly preventative)

What does it treat ?

A

-Quinine & chloroquine

-malaria

112
Q

Where is artemisinin harvested from ?

A

A plant

113
Q

What does artemisinin kill ?

A

Kills plasmodium that causes malaria

114
Q

What is the standard for most parasitical infections and C. Dif?

A

Metronidazole (flagyl)

115
Q

What does metronidazole (flagyl) interfere with?

A

-interferes with anaerobic bacteria

116
Q

What does metronidazole treat?

A

-Trichomonas
-giardiasis
-amebic dysentery

117
Q

Some anti Helminthic drugs?

A

-niclosamide
-praziquantel
-mebendazole & albendazole
-ivermectin

118
Q

What does niclosamide do?
What does it treat?

A

-prevents ATP
-treats tapeworms

119
Q

What does praziquantel do ?
What does it treat ?

A
  • alters membrane permeability
    -treats tapeworms & flukes
120
Q

What does mebendazole & albendazole do ?
What does it treat ?

A

-interfere with nutrient absorption

-treat intestinal helminths

121
Q

What does ivermectin do?

What does it treat?

A

-paralysis of helminths

-treats roundworms and mites

122
Q

What can lead to antibiotic resistance ?

A

-a variety of mutations

123
Q

Resistance genes are often on ______________ or ___________ that can be transferred between bacteria.

A

-plasmids
-transposons

124
Q

How does antibiotic resistance work ?

A

Can get resistance from a plasmid gene because bacteria multiplies fast and has many generations it can mutate easier.

Usually when a DNA is altered so is a protein

125
Q

What is the mechanism of resistance?

A
  1. Blocking entry
  2. Inactivation by enzymes
  3. Alterations of target molecule
  4. Effluent of antibiotic
126
Q

Resistant antibiotic genes can form eflux pump that inactivate?

A

-Penicillin
-molecule

127
Q

Mechanisms of resistance (additional)

A

-enzymatic destruction or inactivation of the drug
-prevention of penetration to the target site within the microbe (any protein blocking drug)
-alteration of the drug’s target site (adding molecule; unrecognizable)
-variations of mechanism

128
Q

Does mycoplasma have a cell wall?

What is it resistant to ?

A

-does NOT have cell wall

-resistant to penicillin

129
Q

Define Persister cells

A

-microbes with genetic characteristics allowing for their survival when exposed to an antibiotic

130
Q

Define superbug

A

Bacteria that are resistant to large numbers of antibiotics

131
Q

How are resistant genes often spread ?

A

Horizontally among bacteria on plasmids or transposons via conjugation or transduction

132
Q

Does someone need to finish antibiotics even if they fell better?

A

-Yes, so a persons immune system can get rid of microbes while antibiotics keep levels low

133
Q

What are some misuses that create antibiotic resistance ?

A

-using outdated or weakened antibiotics
-using antibiotics for the common cold and other inappropriate conditions
-using antibiotics in animal feed
-failing to complete prescribed regimen
-using someone else’s leftover prescriptions

134
Q

Define synergism

A

The effect of 2 drugs together is GREATER than the effect of either alone

135
Q

Define antagonism

A

The effect of two drugs together is less than the effect of either one

136
Q

Give example of antagonism

A

Organism that is treated with penicillin and treated with protein synthesis

137
Q

Define efficacy

A

-safety & factors involved; how much needed to work

138
Q

Another name for disk-diffusion method

A
  • Kirby-Bauer test
139
Q

What does the disk-diffusion method do ?

A

-Tests the effectiveness of chemotherapeutic agents
*paper disks s with a chemotherapeutic agent are placed
agar containing organism

 *zone of inhibition - around the disk determines the sensitivity of the organism to the antibiotic
140
Q

What determines the sensitivity of the organism to the antibiotic ?

What is this method called ?

A

-zone of inhibition

  • Disk-diffusion method (Kirby-Bauer test)
141
Q

What is done with the zone of inhibition ?

A

-diameter is measured and compared to chart to see if it is acceptable

142
Q

What does the E TEST determine?

A

-determines the minimal inhibitory concentration (MIC)
*lowest antibiotic concentration preventing bacterial growth

143
Q

What does the dilution test determine?

A

-determines the MIC and minimal bactericidal concentration(MBC) of an antimicrobial drug

-test organism is placed into the wells of a tray containing dilutions of a drug; growth is determined

144
Q

What are antibiograms ?

A

Reports that record the susceptibility of organisms encountered clinically

145
Q

What are examples of the future of chemotherapeutic agents?

A

-target virulence factors
-sequester iron, which feeds pathogens
-antimicrobial peptides produced by various organisms
-phage (bacterial virus) therapy -bacteria viruses do not harm humans
-bacteriocins: antimicrobial peptides produce by bacteria

Bio 55 (19 decks)

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