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Microbiology Unit 2 > (9-23) Antimicrobial Medications > Flashcards

(9-23) Antimicrobial Medications Flashcards

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1
Q

What did Paul Ehrlich discover in 1910?

A

He discovered that an arsenic-containing compound was effective against Treponema pallidum (the causative agent in Syphilis).

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2
Q

What did Gerhard Domagk discover in 1932?

A

He discovered that Prontosil was effective against Streptococcus. [The breakdown product, sulfanilamide, was active.]

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3
Q

What was the first sulfa drug?

A

Prontosil

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4
Q

What is the definition of an antimicrobial drug?

A

A chemical that inhibits the growth of, or kills, microorganisms.

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5
Q

What is an antibiotic?

A

An antimicrobial drug naturally produced by mold or bacteria.

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6
Q

What did Andrew Fleming discover in 1928?

A

He discovered that mold Penicillium produced a substance (termed “penicillin”) that killed bacteria.

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7
Q

Mass production of which drug saved many soldiers’ lives during WWII?

A

Penicillin

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8
Q

What is one example of a semisynthetic antibiotic?

A

Penicillin

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9
Q

What does selective toxicity mean?

A

Antibiotics cause greater harm to microorganisms than to human host.

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10
Q

How does selective toxicity cause greater harm to microorganisms than to the human host?

A

By interfering with biological structures or biochemical processes common to bacteria, but not to humans.

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11
Q

How is the toxicity of a drug expressed?

A

As a therapeutic index

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12
Q

How is the therapeutic index of a drug calculated?

A

The lowest dose toxic to a patient divided by dose typically used for treatment (high therapeutic index = less toxic to patient).

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13
Q

What is an antimicrobial’s spectrum of activity?

A

Antimicrobials vary with respect to the range of organisms controlled.

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14
Q

Explain and give examples of 2 spectrums of antibiotics.

A
  1. Narrow spectrum: works on a narrow range of organisms
    ~ ex. G+ or G- bacteria ONLY
  2. Broad spectrum: work on a broad range of organisms
    ~ ex. G+ and G- bacteria
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15
Q

What is the disadvantage of broad spectrum antibiotics?

A

Disruption of normal flora

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16
Q

What is antimicrobial action?

A

Drugs may kill or inhibit bacterial growth.

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17
Q

When a drug’s action is to inhibit bacterial growth, it is termed what?

A

Bacteriostatic

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18
Q

When a drug’s action is to kill bacteria, it is termed what?

A

Bacteriocidal

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19
Q

What are the 6 mechanisms of action of antibacterial drugs?

A
  1. Selective toxicity
  2. Inhibition of cell wall synthesis
  3. Inhibition of protein synthesis
  4. Inhibition of metabolic pathways
  5. Inhibition of nucleic acid synthesis
  6. Interference with cell membrane integrity
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20
Q

Why can antibiotics inhibit cell wall synthesis?

A

Eukaryotes lack cell walls

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21
Q

Why can antibiotics inhibit protein synthesis?

A

Ribosomal differences
~ Prokaryotic = 70s ribosome
~ Eukaryotic = 80s ribosome

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22
Q

Why can antibiotics inhibit metabolic pathways?

A

It utilizes those that are different or lacking in eukaryotes

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23
Q

Why can antibiotics inhibit nucleic acid synthesis?

A

Prokaryotic enzymes are different than eukaryotic enzymes

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24
Q

Why can antibiotics interfere with cell membrane integrity?

A

They can bind to the membrane

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25
What level of therapeutic index do Cell Wall Synthesis inhibiting drugs have?
Very high
26
Which organisms do Cell Wall Synthesis inhibiting drugs affect and what are they effective against?
1. Only affect prokaryotes | 2. Only effective in actively growing bacteria
27
What type of drug are β-Lactams?
Cell Wall Synthesis inhibiting
28
What are 2 classes of β-Lactam drugs?
1. Penicillins | 2. Cephalosporins
29
Are β-Lactam drugs more effective against Gram postive or negative bacteria?
Gram positive
30
How do β-Lactam Drugs inhibit Cell Wall Synthesis?
They inhibit enzyme that forms peptide side chains between NAG-NAM chains of peptiodglycan.
31
How can Semisynthetic versions of β-Lactam Drugs better fight bacteria? List 2 ways, with an exmple of each.
1. Semisynthetic versions can be broad spectrum ~ ex Ampicillin 2. Semisynthetic versions “resist” β-lactamase ~ ex. Methicillin)
32
What enzyme contributes to bacterial resistance of β-Lactam Drugs?
Resistance is commonly by β-lactamase enzyme
33
Which bacterial anatomical feature does Vancomycin affect, and what is its mode of operation?
Vancomycin binds NAM, inhibiting synthesis of chains, thereby inhibiting cell wall synthesis.
34
Which bacterial anatomical feature does Bacitracin affect, and what is its mode of operation?
interferes with transport of cell wall precursors
35
Aminoglycosides are in which class of drugs? What is an example of an Aminoglycoside?
They are the Protein Synthesis Inhibition drugs | ~ ex, streptomycin
36
What are Aminoglycosides not effective against, and why?
Anaerobes | ~ Aminoglycosides are actively transported into cell by process that requires respiratory metabolism
37
What do Aminoglycosides do, once they are actively transported into the cell?
They irreversibly binds to 30S ribosomal subunit, blocking initiation of translation
38
Which type of drug are Aminoglycosides often often used in combination with?
β-lactam drugs
39
How does a bacterium gain resistance against a Protein Synthesis Inhibition drug?
Resistance is via a single point mutation in the gene that codes for the protein portion of 30S ribosome
40
Which type of drug is most useful in inhibiting Metabolic Pathways, and what do they do?
Folate Inhibitors | ~inhibit the production of folic acid
41
Sulfonamides and Trimethoprim belong to which class of antimicrobial?
Metabolic Pathway Inhibition drugs
42
How do Sulfonamides (sulfa drugs) work?
They competitively inhibit the enzyme that aids in production of folic acid [Human cells lack enzyme –> selective toxicity]
43
How does Trimethoprim work?
It inhibits the enzyme that humans have, but enzymes are different enough so toxicity is low
44
Which drugs Inhibit Nucleic Acid Synthesis? Give one example.
Rifamycins | ~ ex, Rifampin
45
Which type of drug is effective against Mycobacterium?
Rifamycins
46
How do Rifamycins work?
They block prokaryotic RNA polymerase, stopping initiation of transcription
47
Where does resistance against Nucleic Acid Synthesis drugs come from?
Mutation in gene coding for RNA polymerase
48
What are 3 factors that contribute to the limited range of antimicrobials used in treatment of infections caused by M. tuberculosis?
1. chronic nature of disease 2. slow growth 3. waxy lipid in cell wall
49
Why is the cell wall of M. tuberculosis waxy, and in which way does that enhance the bacterium's ability to resist antibiotics?
Waxy cell wall due to mycolic acid is impervious to many drugs
50
Which 2 drugs are effective against M. tuberculosis? How do they operate?
1. Rifampin ~ blocks RNA polymerase, stopping initiation of transcription 2. Isoniazid ~ inhibits synthesis of mycolic acid
51
Which antiviral medications eliminate latent virus?
NONE of them.
52
What are 3 possible targets of antiviral medications?
1. Polymerase inhibitors 2. Viral uncoating 3. Neuraminidase inhibitors
53
How do the Viral uncoating Antiviral Medications, Amantadine and Rimantadine work, and against which virus?
They block uncoating of influenza virus after it enters cell
54
How do the Neuraminidase inhibitor Antiviral Medications, zanamivir and oseltamivir, work, and against which virus?
They block enzyme essential for release of influenza virus (neuraminidase)
55
Which 4 antiviral medications are used against Influenza?
1. amantadine 2. rimantadine 3. zanamivir 4. oseltamivir
56
What are the 2 broad mechanisms of drug resistance?
1. Drug inactivating enzymes | 2. Alteration of target molecule
57
How do Drug inactivating enzymes work?
Some organisms produce enzymes that chemically modify drug | ~ ex. β-lactamase enzyme breaks β-lactam ring of penicillin antibiotics
58
How do alterations of target molecule lead to drug resistance?
Minor structural changes in antibiotic target can prevent binding ~ ex. Changes in ribosomal protein prevents aminoglycosides from binding
59
How can drug resistance be “shared” (transferred)?
vertically or horizontally
60
How do Quinolines work?
They inhibit heme polymerization
61
List 3 examples of Quinolines.
1 Quinine 2. Chloroquine 3. Mefloquine
62
Why does Plasmodium polymerize the Heme group of hemoglobin?
The Heme group is toxic to the parasite.
63
What do Plasmodium digest for energy, and where does it get it?
Plasmodium in RBC digest hemoglobin for energy
64
What part of the hemoglobin does Plasmodium metaboliz, and how does it handlethe rest of the molecule?
1. Able to digest globin part of hemoglobin (protein) but not able to digest the ring-like heme group 2. cross-links all the heme to form the non-toxic polymer hemozoin
65
Which product of Plasmodium erythrocyte invasion is pigmented, and can easily be seen under the microscope?
Hemozoin

Microbiology Unit 2 (13 decks)

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