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Microbiology 2320 > Chapter 12- Drugs, Microbes, Host > Flashcards

Chapter 12- Drugs, Microbes, Host Flashcards

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1
Q

What is the ideal antimicrobial?

A
  1. Easily administered
  2. Selectively toxic
  3. Highly potent
  4. Stable
  5. Soluble in the body’s tissues and fluids
  6. Does not disrupt the immune system or micro flora of the host
  7. Is exempt from drug resistance
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2
Q

Antimicrobial chemotherapy

A

Administer to an infected person a drug that destroys the infectious agent without harming the hosts cell

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3
Q

Antibiotics

A

Substances produced by natural metabolic process of certain microorganisms that can inhibit or destroy other microorganisms

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4
Q

Where do antimicrobials come from? (List 4)

A
  1. Natural or synthetic
  2. Metabolic product of aerobic bacteria and fungi
  3. Normal function is to inhibit the growth of other microorganisms in the same habitat
  4. Most come from bacteria in genera streptomyces and bacillus and molds in genera Penicillium and Cephalosporium
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5
Q

Chemotherapeutic drug

A

Any chemical used in the treatment, relief or prophylaxis of a disease

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6
Q

Prophylaxis

A

use of the drug to prevent imminent infection of a person at risk

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7
Q

Antimicrobial chemotherapy

A

The use of chemotherapeutic drugs to control infection

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8
Q

Antimicrobials

A

All inclusive term for any Michael real drug regardless of origin

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9
Q

Semisynthetic drugs

A

Drugs chemically modified in a lab after being isolated from natural sources

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10
Q

Synthetic drugs

A

The use of chemical reactions to synthesize antimicrobial couples in the lab

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11
Q

Narrow spectrum

A

Limited spectrum

Antimicrobials effective against a limited array of microbial types. Example, a drug effective mainly on gram+ bacteria

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12
Q

Broad spectrum

A

Extended spectrum
Antimicrobials effective against a wide variety of microbial types. Example, a drug effective against both gram-positive and gram-negative bacteria

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13
Q

The goal of drug administration

A

To get an effective amount of drug to the site of infections before it is broken down and excreted

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14
Q

Local or topical therapy

A

External therapy:

For skin surface infections truck is applied directly to infected area

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15
Q

Intravenous administration

A

Systemic Therapy

  1. Introducing the drug directly into a vein by needle or catheter.
  2. Fastest way of a getting a high level of drug but painful and cannot result in a added infection
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16
Q

Intramuscular administration

A
  1. Introduce drug directly into muscle by injection.
  2. Drug reaches peak level in blood in 15 minutes.
  3. painful and has to be done by a professional
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17
Q

Oral administration(PO)

A
  1. Drug is swallowed.
  2. Absorbed into bloodstream through G.I.
  3. Common, simple, painless administration but slow and in efficient.
  4. Only a fraction of drug get to bloodstream and must be administered often. This leads to dosage errors and failure to comply
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18
Q

How are drugs eliminated from the body?

A

There are two methods, metabolic conversion or excretion

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19
Q

Metabolic conversion

A

A different compounds occurs in the liver, this metabolic product is usually inactive

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20
Q

excretion

A

occurs through the kidneys and into the urine. A few pass through the liver into the bile, and then into the feces.

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21
Q

selectively toxic

A

Should kill or inhibit microbial cells without damaging host cells

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22
Q

What is the goal of antimicrobial drugs?

A

To disrupt the cell processes or structures of the microbe. Most interfere with the function of enzymes, or destroy structures that are already there

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23
Q

Antimicrobial drugs are divided into categories based on which cell targets they affect: (list 5)

A

Inhibition If cell wall synthesis.
Interference with cell membrane structure or function.
Inhibition of protein synthesis.
Inhibition of nucleic acid, DNA or RNA, structure and function.
Inhibition of folic acid synthesis

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24
Q

What antimicrobial block the final step of protein cross links in peptidoglycan?

A

Penicillin and Cephalosporin

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25
Q

What antimicrobials interfere with synthesizing the NAM and NAG strands?

A

Vancomycin and Cycloserine

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26
Q

Inhibition of cell wall synthesis

A
  1. Perfect mode of action since peptidoglycan is unique to bacteria.
  2. Active cells are constantly make a new peptidoglycan
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27
Q

Interference of cell membrane: (list 4)

A
  1. not the best site of action since every cell has some kind of membrane.
  2. Often specificity is for types of lipids within cell membranes.
    3 best if use topically
    4.If used systematically it comes with serious side effects, fever, chills, vomiting, and kidney failure
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28
Q

Polymyxin

A

Interact with membrane phospholipid and distort the cell surface.
Cause seepage of liquids, proteins, and ions.

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29
Q

Polyene Antifungal Antibiotics

A

Form complexes with sterols on fungal membranes. These complexes formed passageways.
Causes seepage of liquids, proteins, and ions
Example: Amphotericin B and Nystatin

30
Q

Inhibition of protein synthesis

A
  1. The side of action is that the ribosome-mRNA complex.

2. the selective toxicity is achievable because of the differences between prokaryotic and eukaryotic ribosomes.

31
Q

Name 5 types of inhibitors of protein synthesis?

A
  1. Streptomycin
  2. Gentamicin
  3. Tetracyclines
  4. Chloramphenicol
  5. Erythromycin
32
Q

Streptomycin and gentamicin

A

Cause the misreading of the mRNA , which equals abnormal proteins

33
Q

Tetracyclines

A

Block attachment of tRNA to the A site, which stops protein synthesis

34
Q

Chloramphenicol

A

Prevents peptide bond formation

35
Q

Erythromycin

A

Prevents movement of ribosome along mRNA

36
Q

Targeting nucleic acids

A

Both prokaryotic and eukaryotic cells contain Nucleus acids. Some enzymes are different enough that we can have enough selective toxicity to be effective. Examples Rifampin and Quinolones

37
Q

Rifampin

A

Inhibits bacterial RNA polymerase

38
Q

Quinolones

A

Inhibition a microbial topoisomerase

39
Q

Inhibiting folic acid synthesis

A
  1. Good selective toxicity, because we don’t manufacture folic acid.
  2. Competitive inhibition Sulfonamides and Trimethoprim inhibit folic acid synthesis.
  3. Given together they provide synergistic effect.
40
Q

Penicillins

  1. antibiotic or synthetic
  2. mode of action
  3. spectrum
  4. Fact
A
  1. Both antibiotics and semisynthetic
  2. inhibits cell wall
  3. narrow spectrum
  4. Penicillins share the same basic structure and differ in the R group attached
41
Q

What kind of problems do you face with penicillin?

A
  1. Allergies and resistant pathogens.
  2. Example: beta lactamase enzymes destroy the beta lactam ring.
  3. Clavulanic Acid inhibits these enzymes. Often added to these drugs. Clavamox a.k.a. Augmentin
42
Q

What is the difference between cephalosporin and penicillin?

A

Penicillin has a five carbon ring and cephalosporin has six carbon ring.

43
Q

Cephalosporins

  1. antibiotic or synthetic
  2. mode of action
  3. spectrum
  4. Fact
A
  1. Both, antibiotics and semisynthetic
  2. Inhibits cell wall
  3. Narrow spectrum
  4. More resistant against beta lactamases and can still cause some allergic reaction like penicillin.
44
Q

Vancomycin

  1. antibiotic or synthetic
  2. mode of action
  3. spectrum
  4. Fact
A
  1. Antibiotic
  2. Inhibits cell wall
  3. Narrow spectrum
  4. Most effective in treating Staph in cases of resistance (penicillin, methicillin) or in those allergic to penicillins. It is very toxic (kidneys), must be administered intravenously.
45
Q

What antibiotics are synthesized from streptomyces? (4)

A

Amino-glycosides
Tetracycline
Chloramphenicol
Erythromycin

46
Q

Aminoglycosides

  1. antibiotic or synthetic
  2. mode of action
  3. spectrum
  4. Fact
A
  1. Antibiotics and a few semisynthetic.
  2. Inhibits protein synthesis.
  3. Narrow spectrum.
  4. Poor absorption when taken orally so must be injected and it can be very toxic. Also is resistance can be developed very easily, often given a combination with other drugs.
47
Q

Streptomycin

A

Oldest but still the drug of choice for bubonic plague and considered a good antituberculosis agent.

48
Q

Gentamicin

A

It’s less toxic and it’s wildly administered for infections caused by Gram-‘s

49
Q

Chloramphenicol

  1. antibiotic or synthetic
  2. mode of action
  3. spectrum
  4. Fact
A
  1. Antibiotic now made synthetically
  2. Inhibit protein synthesis.
  3. Broad spectrum
  4. Doesn’t cause allergies, penetrates tissues, effective when taken internally, can be stored without refrigeration and has few side effects. Once thought to be ideal. Major: rare causes aplastic anemia. Now are used to treat seriously ill and hospitalized patients
50
Q

Tetracyclines

  1. antibiotic or synthetic
  2. mode of action
  3. spectrum
  4. Fact
A
  1. Antibiotics and semisynthetics.
  2. Inhibits protein synthesis.
  3. Broad-spectrum.
  4. Well absorb the orally few allergies occur. However they do not penetrate the blood/brain barrier. Has several side effects which include Gastrointestinal pain and diarrhea, increased sensitivity to sunlight, and can stain developing teeth. Widely used in livestock feed, which caused resistant strains.
51
Q

Erythromycin

  1. antibiotic or synthetic
  2. mode of action
  3. spectrum
  4. Fact
A
  1. Antibiotic.
  2. Inhibits protein synthesis.
  3. Narrow spectrum.
  4. Discovered in 1952, widely used to treat strep throat and other respiratory infections. However resistant S. pyogenes strains have emerged. Easily oral administered but side effects include nausea, vomiting, and stomach pain.
52
Q

Quinolones

  1. antibiotic or synthetic
  2. mode of action
  3. spectrum
  4. Fact
A
  1. Synthetics.
  2. Inhibit DNA replication binds to topoisomerase.
  3. Broad spectrum.
  4. Relatively new group of drugs, easily administered orally, with a few side effects. Drug resistance is not common. Example Ciprofloxacin
53
Q

What drug is used in the anthrax scare?

A

Ciprofloxacin

54
Q

Antimycobacterial Drugs

  1. antibiotic or synthetic
  2. mode of action
  3. spectrum
  4. Fact
A
  1. Synthetic and semi synthetic.
  2. Inhibits protein synthesis. (Rifampin) Inhibits mycolic acids in cell wall. (Isoniazid, Ethambutol)
  3. Narrow spectrum.
  4. Mycolic acid layer nearly impermeable. Mycobacteria Grow slowly, combination of drug have to be used, intracellular pathogen.
55
Q

Why are mycobacteria difficult to treat? (4)

A
  1. Mycolic acid layer nearly impermeable
  2. Mycobacteria grow slowly.
  3. Resistant strain develop readily, combination of drugs must be used.
  4. Intracellular pathogen
56
Q

Antiprotozoan

A

Metronidazole

-Treat giardia

57
Q

Antimalarial

A

Quinine

-malaria

58
Q

Antihelminthic

A

Mebendazole

-tapeworms, round worms

59
Q

What do effective antiviral drugs do?

A

Target viral replication cycle.

  1. Entry.
  2. Nucleic acid synthesis.
  3. Assembly/release
60
Q

What is interferon?

A

Artificial antiviral drug

61
Q

Why are antivirals difficult

A

It’s hard to maintain selective toxicity

62
Q

Antifungal agents

  1. antibiotic or synthetic
  2. mode of action
  3. spectrum
  4. Fact
A
  1. Antibiotics and synthetics.
  2. Inhibit cell membrane, inhibits protein synthesis, inhibits cell division.
  3. Narrow spectrum.
  4. Selective toxicity focuses on Funko sterile’s and cell membrane. Difficult challenges because they’re eukaryotic. Example: Nystatin, Imidazoles & Triazoles, Griseofulvin.
63
Q

Nystatin

A

Usually topical, Candida albicans

64
Q

Imidazoles & Triazoles

A

Can be used topically or systematically instead of Amphotericin B (serious side effect)

65
Q

Griseofulvin

A

Persistent ringworm infection

66
Q

Natural resistance

A

the cell may lack the target the drug attacks, or naturally repel/block the drug

67
Q

Acquired resistance

A

When strains become drug resistant due to mutation or genetic exchange

68
Q

Three mechanisms of resistance

A

Acquiring enzymes that inactivate or destroy the drug (beta-lactamase).

  1. Changing the cellular target.
  2. Excluding the drugs or removing it once it has entered. (N. Gonorrhea)
69
Q

What leads to antibiotic resistant

A

Abuse and miss use of antibiotics

70
Q

What are six ways to slow resistance?

A
  1. Limit nonmedical use of antibiotics, livestock feed.
  2. Stop prescribing anti-bacterial or viral infections.
  3. Stop selling antibiotics without prescription.
  4. Stop prescribing too often or indiscriminately.
  5. Use combined therapy to drugs at once to ensure effectiveness.
  6. Encourage patient compliance.
71
Q

How does resistance develop?

A
  1. Spontaneous mutations in critical chromosome your genes.
  2. Acquisition of new genes or sets of genes from another species.
  3. Natural selection.
72
Q

What happens when antimicrobial drugs is added and kills off all the sensitive organisms.

A

Resistance survivors can multiply without competition

Microbiology 2320 (9 decks)

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