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ANS 302: Veterinary Microbiology > Antimicrobial Chemotherapy > Flashcards

Antimicrobial Chemotherapy Flashcards

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1
Q

What are chemotherapeutic agents?

A

Chemical agents used to treat disease by inhibiting the growth of or destroying the pathogenic microbe.

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2
Q

What are most chemotherapeutic agents classified as?

A

Antibiotics.

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3
Q

Who accidentally discovered penicillin in 1928?

A

Dr. Alexander Fleming.

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4
Q

How was penicillin discovered?

A

A ring of inhibition was observed around mold that had grown on a petri dish left on a lab counter.

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5
Q

When did penicillin become commercialized?

A

Early 1940’s.

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6
Q

What is selective toxicity?

A

The ability of a drug to inhibit or kill pathogens while damaging the host as little as possible.

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7
Q

What is the therapeutic dose?

A

The drug level required for clinical treatment.

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8
Q

What is toxic dose?

A

The drug level at which the drug becomes too toxic for the patient/produces side effects.

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9
Q

What is therapeutic index?

A

The ratio or difference of toxic dose to therapeutic dose.

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10
Q

What are side effects?

A

Undesirable effects of drugs on host cells.

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11
Q

What are narrow spectrum drugs?

A

Drugs that attack only a few different pathogens.

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12
Q

What are broad-spectrum drugs?

A

Drugs that attack many different kinds of bacteria.

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13
Q

What are the 2 ways to measure the effectiveness of a drug?

A
  1. Minimal inhibitory concentration.
  2. Minimal lethal concentration.
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14
Q

What is minimal inhibitory concentration?

A

The lowest conc. of a drug that prevents growth of the pathogen.

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15
Q

What is minimal lethal concentration?

A

The lowest conc. of a drug that kills the pathogen.

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16
Q

What are the 4 modes of action for antimicrobial drugs?

A
  1. Metabolic antagonists.
  2. Inhibitors of cell wall synthesis.
  3. Protein synthesis inhibitors.
  4. Nucleic acid synthesis inhibitors.
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17
Q

What type of bacteria would cell wall synthesis inhibitors work best against, G+ or G-? Why?

A
  1. G+.
  2. Due to having a large peptidoglycan cell wall.
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18
Q

What mode of action does penicillin display?

A

Cell wall synthesis inhibitor.

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19
Q

What are most penicillins?

A

6-aminopenicillanic acid derivatives.

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20
Q

What makes each penicillin different?

A

The side chain attached to the amino acid group.

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21
Q

What is the most critical feature of penicillins? Why?

A

a. The B-lactam ring.
b. It is essential for the bioactivity of the penicillin.

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22
Q

What are the 2 ways penicillin interferes with cell wall synthesis?

A
  1. Blocks transpeptidase.
  2. Prevents the synthesis of a complete cell wall, leading to cell lysis.
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23
Q

What is a limit of cell wall synthesis inhibitors?

A

Can only act on bacteria actively synthesizing a new cell wall.

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24
Q

What defense have some bacteria developed to counter penicillins?

A

B-lactamase/penicillinase.
*Why B-lactamase inhibitors are included with penicillins.

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25
Q

Which type of penicillin has a broader spectrum: natural or semisynthetic?

A

Semisynthetic.

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26
Q

What is the mode of action of cephaolsporin?

A

Cell wall synthesis inhibitor.

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27
Q

What other drug is cephalosporin structurally and functionally similar to?

A

Penicillins.

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28
Q

Is cephalosporin broad-or narrow-spectrum?

A

Broad-spectrum.

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29
Q

What is the mode of action of vancomycin?

A

Cell wall synthesis inhibitor.

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30
Q

What type of antibiotic is vancomycin?

A

Glycopeptide antibiotic.

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31
Q

What two genera of bacteria is vancomycin important in treating?

A
  1. Staphylococcus.
  2. Enterococcus.
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32
Q

What was the name for vancomycin when it came to fighting G+ infections?

A

Drug of last resort, due to not being used as frequently.
*However, resistance is on the rise.

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33
Q

What do protein synthesis inhibitors target, generally?

A

The bacterial ribosome.

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34
Q

What 4 steps of protein synthesis do protein synthesis inhibitors target?

A
  1. Aminoacyl-tRNA binding.
  2. Peptide bond formation.
  3. mRNA reading.
  4. Translocation.
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35
Q

How do protein synthesis inhibitors not interfere with protein synthesis in host cells?

A

Bacterial ribosomes are slightly smaller than the ribosomes of other organisms and are structurally different.

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36
Q

What is unique about protein synthesis inhibitors?

A

Many are bacteriostatic, not bactericidal.

37
Q

What part of protein synthesis do aminoglycosides interfere with?

A

mRNA reading via binding to the 30s ribosomal subunit, causing misreading and miscoding.

38
Q

What part of protein synthesis do tetracyclines interfere with?

A

mRNA reading via binding to the 30s ribosomal subunit, causing misreading and miscoding.

39
Q

Are tetracyclines broad-or narrow-spectrum?

A

Broad-spectrum.

40
Q

What part of protein synthesis do macrolides interfere with?

A

Peptide bond formation via binding to the 50s ribosomal subunit, preventing bacterial protein elongation.

41
Q

Are macrolides broad-or narrow-spectrum?

A

Broad-spectrum.

42
Q

What are the two ways an antibiotic can be metabolic antagonists?

A
  1. Act as antimetabolites.
  2. Act as structural analogs.
43
Q

What are antimetabolites?

A

Substances that antagonize or block the functioning of metabolic pathways by competitively inhibiting the use of metabolites by key enzymes. TLDR: Siphoning gas out of the car.

44
Q

What are structural analogs?

A

Molecules that are similar to, and compete with, naturally occurring metabolic intermediates to block normal cellular metabolism. TLDR: Sitting in the driver’s seat.

45
Q

What is the mode of action of sulfonamides?

A

Metabolic antagonists.

46
Q

What do sulfonamides act as: antimetabolites or structural analogs?

A

Selectively toxic structural analog.

47
Q

What part of the metabolic pathway is a sulfonamide related to?

A

The para aminobenzoic acid (PABA) .

48
Q

What is PABA used for?

A

The synthesis of folic acid and is made in many pathogens.

49
Q

What is the mode of action of trimethoprim?

A

Metabolic antagonist.

50
Q

What does trimethoprim act as: an antimetabolites or a structural analogs?

A

Antimetabolites.

51
Q

Is trimethoprim broad-or narrow spectrum?

A

Broad-spectrum.

52
Q

What other metabolic antagonist does trimethoprim normally combine with to increase efficacy?

A

Sulfonamides.

53
Q

What are the main targets of nucleic acid synthesis inhibitors?

A
  1. RNA polymerase,
  2. DNA polymerase.
  3. Topoisomerase.
54
Q

Why are nucleic acid synthesis inhibitors less selectively toxic than other antibiotics?

A

Due to bacteria and eukaryotes sharing very similar or the same mechanisms for synthesizing nucleic acids.

55
Q

What is the mode of action of fluoroquinolones?

A

Nucleic acid synthesis inhibitor.

56
Q

What enzymes in nucleic acid synthesis do fluoroquinolones inhibit?

A
  1. DNA topoisomerase II.
  2. DNA gyrase.
57
Q

Is fluoroquinolone broad-or narrow-spectrum?

A

Broad-spectrum.
*Bactericidal.

58
Q

Why is drug development slow for viruses?

A

It is difficult to specifically target viral replication due to it happening in a host cell. Additionally, the virus itself does not have much to target as well.

59
Q

What are most antiviral drugs able to do?

A

Either limit the duration of the illness or decrease its severity.

60
Q

Currently, what do most antiviral drugs target?

A
  1. Virus-specific enzymes.
  2. Virus-specific life cycle processes.
61
Q

What are neuraminidase inhibitors used to combat?

A

Influenza, shortening the course of the illness.

62
Q

How do neuraminidase inhibitors function?

A

They prevent the host cell from detaching from the virus following budding, preventing further infection and allowing for the immune system to more easily attack the virus.

63
Q

What drug is used to combat viruses in the genus Herpesviridae?

A

Nucleic acid inhibitors.

64
Q

What type of genome do members of the genus Herpesviridae have?

A

A DNA genome.

65
Q

How do members of the genus Herpesviridae phosphorylate nucleotides?

A

Utilizing their own enzymes.

66
Q

What do nucleic acid inhibitors act as?

A

Nucleoside analogs.

67
Q

What is the mode of action of nucleoside analogs?

A

Incorporate into the viral genome after phosphorylation and block the synthesis of viral DNA.

68
Q

What are the 2 types of reverse transcriptase inhibitors?

A
  1. Nucleoside reverse transcriptase inhibitor (NRTIs).
  2. Nonnucleoside reverse transcriptase inhibitor (NNRTIs).
69
Q

What are 2 examples of reverse transcriptase inhibitors?

A
  1. Nucleoside/-tide inhibitors.
  2. Nucleoside analogs.
70
Q

What is the mode of action of NRTIs?

A

Target and interfere with critical steps in viral replication processes.

71
Q

What is the mode of action of NNRTIs?

A

Prevents DNA synthesis by selectively binding to and inhibiting the viral reverse transcriptase enzyme.

72
Q

What are the different antiviral drug types used to treat HIV?

A
  1. Entry inhibitor.
  2. Fusion inhibitor.
  3. Integrase inhibitor.
  4. Protease inhibitor.
73
Q

What is the mode of action of entry inhibitors?

A

Prevents HIV from binding by altering or blocking receptors.

74
Q

What are 3 examples of entry inhibitors?

A
  1. CCR5 antagonists.
  2. Attachment inhibitors.
  3. Post-attachment inhibitors.
75
Q

What is the mode of action of protease inhibitors?

A

Blocks the activity of the HIV protease needed for the production of all viral protein.

76
Q

What is the mode of action of integrase inhibitors?

A

Prevents the incorporation of the HIV genome into the host’s genome by inhibiting the enzyme integrase.

77
Q

What is the mode of action of fusion inhibitors?

A

Prevents HIV from fusing with the extracellular receptors and entering the cell via endocytosis.

78
Q

Why is a drug cocktail used to treat HIV?

A

Due to how rapidly HIV mutates because of changing from RNA to DNA to RNA.

79
Q

Why are there fewer effective antifungal drugs?

A

Due to the similarity between eukaryotic fungal cells and human cells leading to a low therapeutic index.

80
Q

Which is easier to treat: A superficial mycoses or a systemic mycoses?

A

Superficial mycoses.
*Topical and oral drugs.

81
Q

What is the mechanism of action for antiprotozoan drugs?

A

Not precisely known.

82
Q

What drugs can be used to treat protozoan infections?

A
  1. Those that inhibit protein synthesis in bacteria.
  2. Quinine (Chloroquine and mefloquine).
  3. Metronidazole (Entamoeba infection).
83
Q

What are the 3 types of drug resistance?

A
  1. Intrinsic.
  2. Acquired.
  3. Drug-tolerant bacteria (presisters).
84
Q

What does intrinsic resistance look like?

A
  1. They naturally contain something that makes them resistant, such as a beta-lactam ring.
  2. They lack something that the antibiotic targets, such as a thick enough cell wall.
85
Q

What does acquired resistance look like?

A

A change to the genome occurs that makes a previously susceptible bacteria resistant.

86
Q

What does drug-tolerant resistance look like?

A

Lack the mechanisms to resist the antibiotic and ignore the presence of the antibiotic.
*May be in a biofilm or growing too slowly.

87
Q

What are 4 mechanisms of drug resistance?

A
  1. Drug inactivation.
  2. Modify the target of the antibiotic.
  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. Second one means antibiotic does less damage to the cell.
88
Q

What are three ways to combat drug resistance?

A
  1. Give the drugs in the appropriate concentrations to destroy susceptible microbes and most spontaneous mutations.
  2. Give 2+ drugs at the same time.
  3. Use drugs only when necessary.
89
Q

What are two proposed alternatives to overcoming drug resistance?

A
  1. Using bacteriophages.
  2. Continue developing new drugs.

ANS 302: Veterinary Microbiology (16 decks)

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