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Microbiology > Lecture 18 - Antimicrobial Medications > Flashcards

Lecture 18 - Antimicrobial Medications Flashcards

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1
Q

what is an antimicrobial?

A

a drug that inhibits growth of or kills microbes

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2
Q

what are specific types of drugs within antimicrobials?

A

antibacterial, antifungal, antiprotozoal, anthelmintic

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3
Q

what is an antiviral?

A

A drug that interferes with viral replication (viruses)

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4
Q

what is an antibiotic?

A

a drug that is naturally made by certain microbes against competing microbes, ex: penicillin made by Penicillium mold

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5
Q

who discovered penicillin made by Penicillium mold?

A

Alexander Fleming in 1928

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6
Q

nowadays, the term “antibiotics” also includes what two things?

A

semisynthetic (eg. amoxicillin) and synthetic (eg. ciprofloxacin) drugs.

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7
Q

are the terms antimicrobials and antibiotics used interchangeably?

A

yes, they are just drugs that are affected by microbes

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8
Q

what are antimicrobials toxicity levels?

A

selective toxicity to microbes

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9
Q

what are the two antimicrobial actions and what do they mean? (-cidal and -static)

A

Kill: -cidal (eg. bactericidal)
Inhibit growth: -static (eg. bacteriostatic)

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10
Q

what are the two spectrums of activity in antimicrobials?

A

-Broad spectrum: effective against MORE than 1 group. Example: Gram-positive and negative bacteria.
-Narrow spectrum: effective against ONLY 1 group. Example: Only Gram-positive or negative.

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11
Q

isoniazid’s only effect mycobacteria (made of waxy mycolic acid). what type of spectrum is this?

A

narrow spectrum

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12
Q

tetracyclines effect Gram-positive, negative, chlamydias, and rickettsias. what type of spectrum is this?

A

broad spectrum

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13
Q

what are the routes of administration of antimicrobials?

A

IV, IM, oral, or topical

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14
Q

antimicrobials are distributed in what way?

A

they can get into tissues. so tissue distribution, metabolism,, and excretion of the drug.

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15
Q

do most drug combinations interact?

A

no

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16
Q

when drug combinations do interact, what are the two effects?

A

-Synergistic: the drugs work better together. Example: sulfa drugs + trimethoprim.
-Antagonistic: the drugs DO NOT work together. Example: tetracycline + penicillin.

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17
Q

do Chlamydias/Rickettsias have cell walls? what are they?

A

no, they do not have cell walls. they are obligate intracellular parasites

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18
Q

can there be adverse effects of antimicrobials? what are they?

A

Yes:
-Allergies, especially penicillins and sulfas
-Toxic side effects: in rare cases, chloramphenicol attacks bone marrow cells causing anemia.
-Suppresses normal microbiota

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19
Q

can bacteria be resistant to antimicrobials?

A

yes

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20
Q

what are two types of resistance to antimicrobials and what do they mean?

A

-Innate: the target isn’t present
-Acquired: resistant due to antibiotic-resistance genes

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21
Q

what are last-resort drugs?

A

last resort, saved, antimicrobials are only used if nothing else works. examples:
-vancomycin for resistant Gram-positives.
-carbapenem for resistant Gram-negatives.

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22
Q

you test a patient’s infection against 10 antibiotics at standard doses and find that three will work for that infection. what is the most important consideration to further narrow down the antibiotic list for your particular patient?
1. whether the drug is -cidal or -static?
2. whether the drug is oral or injected?
3. whether the patient is allergic to the drug?
4. whether the drug is narrow or broad spectrum?

A
  1. whether the patient is allergic to the drug?
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23
Q

how many targets do antibacterial drugs have?

A

5

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24
Q

what are the 5 targets of antibacterial drugs?

A
  1. Cell wall (peptidoglycan) synthesis.
  2. Cell membrane integrity.
  3. Protein synthesis.
  4. Metabolic pathways (folate biosynthesis).
  5. Nucleic acid synthesis.
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25
Q

how do antibacterial drugs target the cell wall?

A

by inhibiting peptidoglycan synthesis, causing cell lysis

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26
Q

what are the 3 categories that stop PG synthesis?

A
  1. B-lactam drugs (B-lactam rings)
  2. Glycopeptide drugs
  3. Bacitracin
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27
Q

what do all three classes that stop PG synthesis do?

A

they all inhibit cross-linking. they all block PG synthesis and they lyse the cell

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28
Q

what do B-lactam drugs consist of?

A

-Penicillin and derivatives
-Cephalosporins (5 generations)
-Others, ex. carbapenems

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29
Q

what do glycopeptide drugs consist of / what is an example of glycopeptide drugs?

A

Vancomycin, which is a last resort drug

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30
Q

what is bacitracin in?

A

in triple antibiotic ointment (neosporin), G+

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31
Q

what is the spectrum of antibiotics targeting cell wall synthesis?

A

the spectrum varies from narrow to broad

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32
Q

is targetting cell wall synthesis cidal or static?

A

Bactericidal since it kills cells by lysis

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33
Q

what is selective toxicity?

A

when the antibiotics kill the pathogenic cells, but not the host cells

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34
Q

what are two resistances of the target cell wall (PG) synthesis?

A
  1. B-lactamases
  2. Alternate target - mecA gene (in MRSA - methicillin-resistant S. aerues).
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35
Q

B-lactase makes these enzymes that kill the B-lactam antibiotics, which is resistance. List the 3 B-lactamase enzymes and what they are resistant to.

A
  1. Penicillinase: kills penicillin.
  2. Extended-spectrum B-lactamases (ESBL): kill penicillin AND cephalosporins.
  3. Carbapenemases: kills penicillin, cephalosporins, AND carbapenems.
    a. NDM-1 (New-Delhi metallo-B-lactamase).
    b. KPC (Klebsiella pneumoniae carbapenemase).
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36
Q

what is the mecA gene in MRSA?

A

When methicillin kills the cells by targeting an enzyme used to build PG crosslinks.
MRSA encodes for an alternate enzyme MecA that is resistant to the action of methicillin.

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37
Q

what are topicals used in cell wall (PG) synthesis target?

A

-Used in a concentrated area - does not diffuse away.
-Contains 3 antibiotics - at least 1 will be effective.
Not usually resistant

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38
Q

Antibiotics also target Plasma Membrane (cell membrane) Integrity. What does is cause?

A

It interferes with the plasma membrane - which causes cell leakage and death

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39
Q

when antibiotic drugs target the cell membrane integrity, does it cause cidal or static?

A

Bacteriocidal

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40
Q

what is the spectrum for plasma membrane integrity?

A

Narrow spectrum

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41
Q

is the plasma membrane integrity target selectively toxic?

A

no - the selective toxicity is not too good

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42
Q

what are examples of drugs that target plasma membrane integrity?

A

-Polymyxin B (triple antibiotic ointment): Gram-negative; topic only (this is the 2nd antibiotic in Neosporin).
-Daptomycin: Gram-positive; specifically binds to bacterial lipids

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43
Q

Antibiotics also target protein synthesis. What does it inhibit?

A

It inhibits protein synthesis by attaching to various subunits of the 70s ribosomes

44
Q

is the target protein synthesis selectively toxic?

A

Yes, it is selectively toxic unless the drug penetrates into the mitochondrion, then it is problem. Because that is where the 70s ribosomes are since it is eukaryotic. Inhibits mitochondrial protein synthesis.

45
Q

why is chloramphenicol not used in protein synthesis target?

A

not used because in rare cases it can penetrate and inhibit mitochondrial protein synthesis - it kills rapidly growing cells like bone marrow cells

46
Q

What are 3 examples of protein synthesis target?

A
  1. Aminoglycosides
  2. Tetracyclines
  3. Macrolides
47
Q

what are two examples of aminoglycosides in protein synthesis?

A

-Gentamicin: Gram-negative; “saved” drug.
-Neomycin: in triple antibiotic ointment (3rd drug in neosporin).

48
Q

what are two examples of tetracyclines? are they narrow or broad?

A

doxycycline and minocycline

49
Q

what are two examples of macrolides?

A

gram-positive: erythromycin, azithromycin (Z pack)

50
Q

examples of protein synthesis can also be new drugs - what are they developed resistant to?

A

Gram-positive

51
Q

what is the spectrum of protein synthesis?

A

narrow to broad

52
Q

is protein synthesis cidal or static?

A

Bacteriostatic except for aminoglycosides

53
Q

what are the direct effects of the drug Gentamicin in targeting protein synthesis?

A

Gentamicin can have toxic side effects on ear cells (causes partial or complete deafness), kidney cells (causes kidney damage)

54
Q

antibiotics can also target metabolic pathways (folate pathway) - what happens here?

A

Folate pathway (only in bacteria) inhibitors: act as substrate analogs to inhibit different parts of the folate pathway which produces nucleotides.

55
Q

what is the folate pathway important for?

A

it is important to make nucleotides for DNA and RNA

56
Q

is the metabolic folate pathway cidal or static?

A

bacteriostatic

57
Q

is the folate metabolic pathway narrow or broad spectrum?

A

broad spectrum

58
Q

what are the two drugs within the folate pathway?

A

Sulfonamides (sulfas): stops the 1st reaction
Trimethoprim: stops the 2nd reaction

59
Q

what is the folate pathway?

A

PABA - Sulfamethoxacole - Dihydrogolic acid - Trimethoprim - Tetrahyrofolic acid (makes folate)

60
Q

what do the drugs do to the folate pathway? why are they called synergists?

A

The drugs block the folate pathway, so no folate is made, and therefore no nucleotides are made.
These drugs are synergists, meaning they are prescribed in combination.

61
Q

why are the drugs that inhibit the folate pathway called substrate analogs/mimics?

A

because they mimic the actually substrate/drugs (?)

62
Q

do humans have the folate pathway?

A

no, only bacteria

63
Q

antibiotics also target nucleic acid synthesis. what exactly does it inhibit?

A

inhibits DNA or RNA synthesis

64
Q

is the nucleic acid synthesis cidal or static?

A

bactericidal

65
Q

is the nucleic acid synthesis broad or narrow spectrum?

A

broad spectrum

66
Q

what are two examples of the nucleic acid synthesis target?

A

-Fluoroquinolones: inhibits DNA gyrase, for example, ciprofloxacin. The DNA doesn’t unwind.
-Metronidazole: binds DNA in anaerobic organisms, causing damaging breaks.

67
Q

A patient has a garden variety (not resistant to anything) Gram-positive sinus infection. What are some reasonable antibiotic choices?
1. Vancomycin, carbapenem
2. Penicillin, macrolides (ex: Z-pack)
3. Gentamicin, colistin
4. Bacitracin, polymyxin B

Extension: What if the infection was due to resistant Gram-positive bacteria?

A
  1. Penicillin, macrolides (ex: Z-pack)

Explanation:
1. Last resort drugs - Vancomycin
2. Gentamicin – G-
3. Bacitracin – topical ointment

Extension: Vancoymcin, carbapenem

68
Q

when antibiotics were discovered, what were they called? why did drug companies have disincentives?

A

They were called magic bullets.
Drug companies has disincentives because it didn’t make them any money.

69
Q

what were the strategies for antibiotics?

A

-Modify old drugs (derivative)
-Develop “out of the box” alternatives including vaccines, phage therapy, look into novel natural habitats like honey and the oceans, gene regulation like siRNAs and quorum sensing, and probiotics.

70
Q

what is sensitive or susceptible bacteria?

A

bacteria that get knocked out by antibiotics

71
Q

what is resistant bacteria?

A

bacteria that survive attack by antibiotics

72
Q

what are 6 of the 18 most alarming antibiotic resistance threats?

A

-Vancomycin-resistant Enterococcus (VRE)
-Carbapenam-resistnat Acinetobacter species (CRAsp)
-Methicillin-resistant Staphylococcus aureus (MRSA)
-Carbapenem-resistant Enterobacterales (CRE)
-ESBL
-Multidrug-resistant (MDR) Pseudomonas aeruginosa

73
Q

what are the 4 ways/mechanisms that bacteria become resistant to antibiotics?

A
  1. Drug-inactivating enzymes
  2. Alteration in target molecule
  3. Decreased uptake of drug
  4. Increased elimination of drug
74
Q

what happens with drug-inactivating enzymes? what is an example?

A

When an enzyme modifies an antibiotic and inactivates it. The antibiotic enters, but can’t bind to the target because it is inactivated.
K. pneumonia carbapenemases (KPCs) can break down carbapenems and other B-lactams.

75
Q

what happens when there is an alteration in the target molecule?

A

When the antibiotic cannot bind to the target. The antibiotic goes into the cell, but the target changes, so it cannot bind to the target, and the antibodies cannot work or inhibit anything.

76
Q

what is an example of alteration in target molecule?

A

mecA in MRSA

77
Q

what happens in the mechanism of decreased uptake of the drug?

A

When the porin proteins prevent antibiotic entry into the cell, by modifying surface transport proteins. (Surface transport proteins are porins.)

78
Q

what happens in the mechanism of increased elimination of the drug?

A

when the antibiotic enters the cell but efflux pump ejects it. It actively pushes the antibiotic out of the cell right when it enters.

79
Q

what are the 2 ways of acquisition of resistance genes? AKA how do bacteria get these resistance genes?

A
  1. Mutations - random changes in gene sequence.
  2. Horizontal gene transfer
80
Q

what are three ways within the horizontal gene transfer that resistance genes get acquired?

A

Transduction: resistance genes being transferred from one microbe to another via phages.
Conjugation: resistance genes being transferred between microbes when they connect using sex pilus
Transformation: resistance genes being released from nearby live or dead germs and picked up directly by another germ.

81
Q

what is the evolution of resistance like? what do antibiotics do?

A

antibiotics “select” resistant bacteria from population - antibiotics are NOT CREATING resistant bacteria, they are SELECTING resistant bacteria

82
Q

how does the usage of antibiotics affect its resistance? how about through infections?

A

The more antibiotics we use, the more prevalent resistant bacteria become.
Resistant bacteria can spread through communities causing deadly infections

83
Q

what are ways resistant bacteria are spread?

A
  • Agriculture: 70% of all antibiotics usage goes into farming - not to stop the infection, but to fatten the animals up and use as a preventative measure.

-Hospitals: immunocompromised people and patients with invasive producers are more susceptible.

-Water, soil, and air

84
Q

what are prevention strategies to not let resistance spread?

A

-Prevent and control infections
-Raise awareness to limit use in humans, other animals, and crops.
-Better diagnostics
-Alternative therapies
-Funding to develop new drugs
-Tracking and regulations
-Better sanitation and access to safe drinking water
-Do your part !!!

85
Q

which type of resistance do carbapenemase-producing enterobacteria represent?
1. Drug-inactivating enzymes
2. Alteration in target molecule
3. Decreased uptake of drug
4. Increased elimination of drug

A
  1. Drug-inactivating enzymes
86
Q

what do antifungal drugs do?

A

-Many antifungal drugs bind or inhibit synthesis of ergosterol in the plasma membrane of fungi (NOT in humans). Ex: clotrimazole

87
Q

within antifungal drugs, can drugs against other targets affect human cells?

A

yes, they might

88
Q

what are antiviral drugs?

A

drugs interfering with viral replication (because we can’t target our own machinery and organelles that viruses use)

89
Q

what is a potential problem with antiviral drugs?

A

that viruses use host machinery to replicate so there are limited targets for the antiviral drug to target

90
Q

what viruses are antiviral drugs only designed for?

A

only designed for viruses causing chronic and severe infections

91
Q

what do antiviral and antifungal medications have in common?
1. There are many drugs available to treat these infections.
2. There are not many targets present that humans don’t have
3. They are only used for chronic illnesses.
4. They are called antibiotics

A
  1. There are not many targets present that humans don’t have
92
Q

Antibiotics that are most likely to disrupt the normal microbiota are termed…

A

Broad spectrum

93
Q

Which of the following bacteria have an innate resistance to penicillin?
1. Streptococcus
2. Mycoplasma
3. Escherichia
4. Bacillus
5. Staphyloccocus

A
  1. Mycoplasma
94
Q

The major class(es) of antibiotics that inhibit protein synthesis include all of the following EXCEPT:
1. bacitracins
2. macrolides
3. tetracyclines
4. streptogramins
5. aminoglycosides

A
  1. bacitracins
95
Q

The most common method of transfer of antimicrobial resistance is through the use of
1. R plasmids
2. Introns
3. Exons
4. Viruses
5. F plasmids

A
  1. R plasmids
96
Q

Antiviral drugs may target all of the following EXCEPT
1. viral ribosomes
2. viral uncoating
3. viral assembly
4. viral entry
5. nucleic acid synthesis

A
  1. viral ribosomes
97
Q

In the presence of penicillin, a Gram-positive bacterial cell dies because:
1. Its outer membrane is disrupted
2. Its protein synthesis is halted
3. Its DNA replication cannot proceed
4. Its incomplete cell wall cannot prevent cell lysis
5. Its folate pathway is inhibited

A
  1. Its incomplete cell wall cannot prevent cell lysis
98
Q

Which of the following drugs are not bactericidal?
1. Tetracyclines
2. Cephalosporins
3. Aminoglycosides
4. Fluoroquinolones
5. Vancomycin

A
  1. Tetracyclines
99
Q

To create penicillin resistance, penicillinase:
1. Increases pumping of penicillin out of the cell
2. Alters porins so penicillin can’t get into the cell
3. Breaks the ß-lactam ring to inactivate penicillin
4. Alters the cell wall target so penicillin can’t bind
5. Increases metabolism of penicillin in the cell

A
  1. Breaks the ß-lactam ring to inactivate penicillin
100
Q

Which of the following antimicrobial agents is recommended for use against fungal infections?
1. Clotrimazole
2. Bacitracin-Polymyxin B-Neomycin
3. Daptomycin
4. Macrolides
5. A Trimethoprim/Sulfa combination

A
  1. Clotrimazole
101
Q

Which of the following is true about antiviral drugs?
1. They include neomycin, bacitracin and polymyxin B
2. They only target viral release from the infected cell
3. They can also kill bacteria
4. They have only been developed for a few chronic and/or deadly viruses
5. They include clotrimazole

A
  1. They have only been developed for a few chronic and/or deadly viruses
102
Q

Would it be better to use a broad spectrum or narrow spectrum antibiotic in the treatment of an infectious disease? Discuss the risks and benefits of each.

A

If you administer a targeted antibiotic (one specific for an infection), the less effect it will have on the normal flora, and the patient will have less of a chance of getting a superinfection. In addition, a targeted antibiotic will affect fewer types of bacteria, so selective pressure for resistance will be decreased. However, this strategy only works if there is a narrow spectrum antibiotic available and if the specific disease causing organism is identified (which takes time). But, early in an infection, the organism has often not been identified. Further, there may be more than one infectious agent at work. Therefore, it may be useful to use a broad spectrum antibiotic that will address the possible infectious agents to get a head start controlling the infection, especially if it is severe or life-threatening.

103
Q

Let’s say an older patient comes to the doctor’s office where you are working as a nurse. He says he started getting a cold yesterday and needs antibiotics. He has gotten them in the past whenever he has had a cold. After doing a physical exam and ruling out serious problems such as strep throat, bronchitis and pneumonia, the doctor tells the patient that he has a common cold and he will start to feel better in about a week. After the doctor leaves the room, the patient becomes visibly upset and asks you why he didn’t get his antibiotics as he has in the past. In your best diplomatic tone, discuss with the patient:
Why antibiotics do not work for a common cold
The importance of appropriate antibiotic use
What the patient can do to get some relief from his cold
What to do if he is not starting to feel better in a week

A

You’ll have to come up with your own diplomatic way of answering this question (and you may want to practice it before you experience this scenario in real life), but here are the main points you will need to get across.
Antibiotics do not work for a common cold because a cold is a virus, and antibiotics only attack bacteria. Traditionally, patients attributed feeling better to antibiotics, when, in fact, it was their own immune systems kicking in at about a week after infection.
Antibiotics must be used appropriately to prevent development of resistance. Antibiotic resistance is on the rise due to overuse (for colds and other viral infections) and misuse (patients not taking them correctly). Eventually, antibiotics may become ineffective if not used appropriately and sparingly. As needed, discourage “antibiotic-seeking” behavior. The patient may threaten to find another doctor who will prescribe antibiotics, but inform him that the current standard of practice for all doctors is to withhold antibiotics for colds.
The patient can get symptomatic relief from his cold by getting plenty of rest, drinking lots of fluids and using a humidifier that moistens the air. He can also discuss over-the-counter cold medicines with the doctor, but be aware that some may have side-effects such as high blood pressure or drowsiness.
If the patient is not starting to feel better in a week or so, he should have a follow-up appointment with the doctor to make sure that a secondary infection has not taken hold. Similarly, if new and more severe symptoms arise at any time such as persistent sore throat, chest pain, difficulty breathing, wheezing, etc., contact the doctor as these could indicate a secondary infection or complication.

104
Q

what is the target of antiviral drugs?

A

The target of anti-viral drugs is anything that is not the host cell machinery - steps in viral replication like entry or release.

105
Q

why does mycoplasma have an innate resistance to penicillin?

A

because penicillin targets the PG cell wall and mycoplasma doesn’t have a cell wall. So it has an innate resistance to penicillin.

Microbiology (53 decks)

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