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Micro > Antimicrobial Drugs and Resistance > Flashcards

Antimicrobial Drugs and Resistance Flashcards

1
Q

What are antimicrobial drugs?

A

Drugs that stop the growth or kill various pathogens

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2
Q

What is an antibiotic?

A

An antibiotic is naturally produced by an organism that works against another organism. It can inhibit or kill bacteria.

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3
Q

What is a semisynthetic antibiotic?

A

A modified version of an antibiotic.

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4
Q

What is a synthetic antibiotic?

A

A drug that is developed in a lab and is not originally found in nature.

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5
Q

What makes a good drug target in a microbe?

A

In a microbe, the different structural features of a cell that are not found in those of humans make them a good drug target.
- For example, the 70S ribosomes in bacteria or the chitin in fungal cell walls.
- These differences make it easier for a drug to fight against a microbe.

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6
Q

What are some characteristics of an ideal antimicrobial drug?

A

A characteristic of an ideal microbial drug is selective toxicity. When an antimicrobial drug has selective toxicity, it can inhibit the growth of microbial targets without harming the normal microbiota in the host.
- Other characteristics of an ideal antimicrobial drug are if it is soluble in body fluids and if resistance to the drug is not likely to occur.

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7
Q

What does broad spectrum mean?

A

the drug targets a variety of different groups of microbes

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8
Q

What does narrow spectrum mean?

A

it targets only a specific group of microbes

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9
Q

What is the problem with broad spectrum antibiotics?

A

Kills off pathogens but also kills off normal microbiota

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10
Q

What is the route of administration based on?

A

Is it soluble or not?
How well does it work? What is the toxicity level?
What is it being used for?

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11
Q

What are the major routes of administration?

A

orally, through an intravenous injection, or an intramuscular injection

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12
Q

What factors determine the route used for an antimicrobial drug?

A

The route depends on the solubility of the drug, how well it works, what it is being used for, and its toxicity level. The route used also depends on the condition of the individual and the type of illnesses that they may have.

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13
Q

What are the beta-lactams?

A
  1. Penicillins
  2. Cephalosporins
  3. Aminoglycosides
  4. Tetracyclines
  5. Macrolides
  6. Lincosamides
  7. Polymyxins
  8. Lipopeptides
  9. Rifamycin
  10. Fluoroquinolones
  11. Sulfonamides
  12. Isoniazid
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14
Q

What are penicillins?

A

NARROW spectrum
- drugs that are primarily active against gram-positive bacterial pathogens and a few gram-negative bacterial pathogens
- act by inhibiting the synthesis of the bacterial CELL WALL

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15
Q

What are examples of penicillins?

A

penicillin G, penicillin V, amoxicillin, ampicillin, and methicillin

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16
Q

What are cephalosporins?

A

NARROW SPECTRUM
- increased gram-negative spectrum than penicillins.
- inhibit bacterial CELL WALL synthesis.

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17
Q

What are examples of cephalosporins?

A
  • cephalosporin C
  • first to fifth generation cephalosporins
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18
Q

What are aminoglycosides?

A

BROAD-SPECTRUM drugs that target and bind to 30S subunits and disrupt protein synthesis. They make the cell produce faulty proteins.

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19
Q

What are examples of aminoglycosides?

A
  • streptomycin
  • gentamicin
  • neomycin
  • kanamycin.
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20
Q

What are tetracyclines?

A

BROAD-SPECTRUM drugs that target and bind to 30S subunits and inhibit protein synthesis. They block protein synthesis by blocking the tRNAs that bring in the amino acids.

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21
Q

What are examples of tetracyclines?

A
  • tetracycline
  • doxycycline
  • tigecycline.
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22
Q

What are macrolides?

A

BROAD-SPECTRUM drugs that target and bind to 50S subunits. They inhibit peptide formation and block the elongation of proteins to stop protein synthesis

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23
Q

What are examples of macrolides?

A
  • erythromycin
  • azithromycin
  • telithromycin.
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24
Q

What are lincosamides?

A

NARROW SPECTRUM drugs that target and bind to 50S subunits. They prevent peptide bond formation and inhibit protein synthesis.

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25
Q

What are examples of lincosamides?

A
  • lincomycin
  • clindamycin
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26
Q

What are polymyxins?

A

NARROW SPECTRUM against gram-negative bacteria including those that are multidrug resistant strains. They disrupt the outer and inner membrane of gram-negative bacteria and kill them

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27
Q

What are examples of polymyxins?

A
  • Polymyxin B and E
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28
Q

What are lipopeptides?

A

NARROW SPECTRUM against gram-positive bacteria including the multidrug resistant strains. It inserts itself in the cytoplasmic membrane of gram-positive bacteria. It disrupts the cell membrane and kills the cell.

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29
Q

What is an example of lipopeptides?

A

daptomycin

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30
Q

What are rifamycins?

A

NARROW SPECTRUM against gram-positive and a limited amount of gram-negative bacteria. It blocks the RNA polymerase activity of bacteria. This blocks transcription and kills the cell.

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31
Q

What are examples of rifamycins?

A

Rifampin

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32
Q

What are fluoroquinolones?

A

BROAD SPECTRUM against gram-positive and negative bacteria. It blocks the replication of DNA and kills the cell.

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33
Q

What are examples of fluoroquinolones?

A
  • ciproflaxin
  • ofloxacin
  • moxifloxacin
34
Q

What are sulfonamides?

A

BROAD SPECTRUM against gram positive and negative bacteria. It targets and blocks folic acid synthesis. It does this by inhibiting the enzyme that is involved in producing dihydrofolic acid.

35
Q

What are examples of sulfonamides?

A
  • sulfamethoxazole
  • dapsone
36
Q

What are isoniazids?

A

NARROW SPECTRUM against mycobacterium spp., including M. tuberculosis. It targets and prevents the synthesis of mycolic acid.

37
Q

What is an example of isoniazids?

A

isoniazid

38
Q

What makes a good drug target in Fungi?

A

its cell membrane and its pathways that synthesize sterols.

39
Q

Why are there fewer targets than in bacteria (fungi)?

A

There are fewer targets because fungi are very similar to human cells. This makes it tougher to develop drugs with selective toxicity. As a result, they are less selectively toxic. They have higher toxicity and a higher side effect rate.

40
Q

What are azoles (Imidazoles, Triazoles)?

A

Imidazoles and triazoles work by disrupting and inhibiting ergosterol synthesis. Triazoles have more selective toxicity than imidazoles.

41
Q

What are polyenes?

A

They create pores that disrupt the membrane when they bind to ergosterol in the cell membrane.

42
Q

What are echinocandins?

A

They block and inhibit cell wall synthesis. Target chitin in fungi cell walls.

43
Q

What makes a good drug target in protozoans?

A

What makes them a good drug target are the structures and processes that they contain that differ from human cells. For example, electron transport in mitochondria, folic acid synthesis, DNA synthesis, and heme detoxification

44
Q

Why are there fewer targets than in bacteria (protozoans)?

A

There are fewer due to their similarity to human cells.

45
Q

What is artemisinin?

A

Their mechanism of action is uncertain, but they are thought to produce reactive oxygen species that damage target cells.

46
Q

What is nitroimidazoles?

A

They interfere with nucleic acid synthesis. They introduce DNA strand breakage and interfere with the DNA replication in target cells.

47
Q

What are quinolines?

A

They interfere with and inhibit heme detoxification.

48
Q

What makes a good drug target in viruses?

A

What makes viruses good drug targets are their proteins, enzymes, and processes that differ from human cells.

49
Q

Why are there fewer targets than in bacteria (viruses)?

A

There are fewer targets because they are obligate intracellular pathogens, and they have a simple structure. This makes it hard to develop drugs that have selective toxicity against viruses.

50
Q

What is acyclovir?

A

Causes chain termination when it is added to a growing DNA strand during replication. It inhibits nucleic acid synthesis.

51
Q

What are antiretrovirals (HIV)?

A

Classes of drugs that are used for the treatment of HIV. A cocktail of three or more of these drugs are taken by a person for treatment.

52
Q

What are reverse transcriptase inhibitors?

A

They block the steps of changing the viral RNA genome into DNA. It blocks HIV from replicating.

53
Q

What are protease inhibitors?

A

They block the processing of viral proteins. They prevent viruses from maturing. New viruses cannot be assembled.

54
Q

What are integrase inhibitors?

A

block the activity of the integration step. They stop HIV integrase from recombining a DNA copy of the viral genome into the chromosome of the host.

55
Q

What are fusion inhibitors?

A

They prevent the binding of HIV to the host cell receptors. They also prevent the merging of the viral envelope with the host cell membrane. As a result, HIV cannot get into the cell.

56
Q

What is natural resistance?

A

When a microbe is naturally resistant to an antibiotic. They did not need a mutation to occur in order to obtain resistance to the antibiotic.

57
Q

What is acquired resistance?

A

When a microbe develops the ability to resist an antibiotic that it was previously susceptible to. This occurs from repetitive exposure to the drug leading to the development of its resistance via a mutation or obtaining DNA from a microbe that was already resistant.

58
Q

What are the mechanisms of acquired drug resistance?

A
  1. drug modification or inactivation
  2. efflux of drug/activation of drug pumps
  3. blocked penetration/decreased permeability of drug
  4. enzymatic bypass (alternate metabolic pathways/target overproduction)
  5. target modification
59
Q

What happens in drug modification or inactivation?

A

Enzymes can chemically modify an antimicrobial drug using hydrolysis. This leads to the inactivation of the drug so it no longer works.

60
Q

What happens in efflux of drug/activation of drug pumps?

A

The number of drug pumps is increased. As a result, even when a drug gets into a cell, it gets pumped out before it can negatively affect the cell.

61
Q

What happens in blocked penetration/decreased permeability of drug?

A

A mutation in the transmembrane protein makes it so the drug can no longer pass through it. Less of the drug is getting into the cell.

62
Q

What happens in enzymatic bypass (alternate metabolic pathways/target overproduction)?

A

A bypass is created to find a way around and overcome the blocking of a pathway.

63
Q

What happens in target Modification (alteration of drug binding site)?

A

A mutation causes a structural change to the target. This prevents drug binding making the drug ineffective.

64
Q

What is MRSA?

A

methicillin-resistant Staphylococcus aureus. They are resistant to all B-lactams. This means it is also resistant to methicillin.
- Methicillin was thought to work effectively against gram-positive bacteria that have beta-lactamase. For this reason, it is concerning that MRSA is resistant against all B-lactams.

65
Q

What is VRE/VRSA and why is it of extra concern?

A

vancomycin-resistant enterococci and vancomycin-resistant S.aureus. Both are resistant to vancomycin. This is of extra concern because vancomycin is one of the last lines of defense against resistant infections like MRSA. If microbes develop resistance against these drugs, it will be more difficult to find a stronger treatment against the disease. There will also be fewer treatment options for the disease.

66
Q

What is MDR?

A

multi-drug resistant Mycobacterium tuberculosis. Its strains are resistant to isoniazid and rifampin. These drugs are usually prescribed to treat tuberculosis.

66
Q

What is XDR?

A

extremely drug-resistant Mycobacterium tuberculosis. These strains are resistant to any fluoroquinolone. It is also resistant to at least one of a total of three other drugs. These include amikacin, kanamycin, or capreomycin. These drugs are often used as a second line of treatment for tuberculosis.

67
Q

What are the different tests for determining the effectiveness of an antimicrobial drug

A
  • Kirby-Bauer disk diffusion
  • antimicrobial susceptibility test
  • Etest
68
Q

What is the Kirby-Bauer disk diffusion test?

A

includes looking for a clear zone of inhibition around a disk. The size of the clear zone shows the resistance of the bacterial pathogen to the drug. This is measured to determine the susceptibility of certain microbes to various antibiotics.

69
Q

What is the antimicrobial susceptibility test?

A

involves the use of a 96-well microdilution tray. The wells contain the drug in low concentration to higher concentration across the twelve wells. In each row, there are different microbial drugs. After growth, turbidity is used to find the MIC. The MIC is shown where the growth from turbid to not turbid.

70
Q

What is the Etest?

A

uses a lawn on a plate. A test strip is placed on the surface of the agar plate. An elliptical zone of inhibition is used to find the MIC. It can be found by looking at where the growth stops.

71
Q

What is MIC?

A

MIC is the minimal inhibitory concentration. It is the lowest concentration of the drug where it can still inhibit bacterial growth.

72
Q

What is happening to the rate of antimicrobial drug discovery? Why?

A

The rate of antimicrobial drug discovery has decreased dramatically. However, drug resistance has increased. There are too few antimicrobial drugs being discovered to keep up with the increasing amount of antimicrobial resistant diseases. Antimicrobial drugs are being overused and misused resulting in increased drug resistance. Discovering new antimicrobial drugs is also time consuming with low success rates. For this reason, the rate of antimicrobial drug discovery has gone down.

73
Q

What does a high mutation rate signify?

A

a higher rate of drug resistance

74
Q

What do all B-lactam drugs have in common?

A

The B-lactam ring

75
Q

What makes the B-lactams different?

A

Their R group

76
Q

What is PABA (normal pathway?

A

Pyramid amino benzoic acid –> enzyme converts it to dihydrofolic acid –> enzyme converts it to tetrahydrochloric acid –> nucleotides

77
Q

What is the sulfonamide pathway?

A

Sulfonamide binds to an enzyme and clogs it up so the enzyme shuts down
- Competitive inhibitor, prevents the real substrate from binding to the enzyme, therefore, blocking that metabolic pathway

78
Q

What is PABA (2)?

A

pyramid amino benzoic acid binds to enzyme and converts it to trimethoprim –> when trimethoprim binds to an enzyme, it clogs it up and shuts it down
- It blocks the pathway the step after sulfonamides

79
Q

IV route of administration

A

Nice high response almost right away
- Requires healthcare professional to be administered

80
Q

IM route of administration

A

Comes up a bit slower
- Requires healthcare professional to be administered

81
Q

Oral route of administration

A

Slower and not quite as high as IV or IM
- Can be incredibly effective because one can give patients a prescription and they can go home

Micro (21 decks)

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