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SMP - MIM Part 2 > Lecture 5 - Antimicrobial Therapy > Flashcards

Lecture 5 - Antimicrobial Therapy Flashcards

1
Q

4 types of antimicrobials?

A
  1. Antibacterial
  2. Antiviral
  3. Antifungal
  4. Antiparasitic
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2
Q

What are 3 non-selective methods to kill microbes? Describe each.

A
  1. Sterilization: killing of ALL microbes present by physical or chemical means
  2. Disinfection: killing of most microbes by chemical or physical means
  3. Antisepsis: use of disinfecting agents that can be applied to the skin
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3
Q

4 examples of sterilization? Do these eliminate bacterial spores?

A
  1. Pressurized steam (121 degrees Celsius, 15 psi)
  2. Plasma gas
  3. Ionizing radiation
  4. Ethylene oxide gas

YUP

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4
Q

3 examples of disinfection?

A
  1. Phenolics
  2. Iodophors
  3. Quarternary ammonium compounds
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5
Q

3 examples of antisepsis?

A
  1. Alcohol
  2. Iodophors
  3. Chlorhexidine
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6
Q

What microbes resist to boiling?

A

Bacterial spores

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7
Q

What is central to the clinical application of antimicrobials?

A

Selective toxicity

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8
Q

Describe the history of the discovery of antimicrobials.

A
  1. 1909: development of the concept of selective toxicity of drugs and of Salvarsan, an arsenical dye, effective against syphilis
  2. 1932: discovery of red dye, prontonsil rubrum, which protected mice and rabbits from infection with staphylococci or streptococci (sulphonamide later shown to be the active component, sulpha drugs still used today)
  3. 1929: discovery of mold, Penicillium notatum, produced substance that killed staphylococci; “penicillin”
  4. 1944: antibiotics term coined = “a compound produced by a microbe that kills or inhibits the growth of another microbe” with discovery of streptomycin from Streptomyces spp., a filamentous bacterium common in soil
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9
Q

3 main microbial sources of antibiotics?

A
  1. Streptomyces species (bacteria)
  2. Cephalosporium species (fungi)
  3. Penicillium notatum (fungi)
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10
Q

6 types of antibiotics from streptomyces species?

A
  1. Tetracycline
  2. Macrolides
  3. Aminoglycosides
  4. Chloramphenicol
  5. Lincosamides
  6. Streptogramins
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11
Q

Type of antibiotics from cephalosporium species?

A

Cephalosporins

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12
Q

Type of antibiotics from penicillium notatum ?

A

Penicillins

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13
Q

What makes some individuals immune to particular microbes?

A

Differences in microbiomes

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14
Q

Definition of antibiotics?

A

Naturally occurring microbial products

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15
Q

Definition of semi-synthetic antibiotics?

A

Chemically modified derivatives of antibiotics

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16
Q

Definition of chemotherapeutic agents?

A

Invented synthetic compounds

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17
Q

2 possible effects of antibacterials? Name of drugs for each?

A
  1. Prevent bacteria from growing = bacteriostatic antibiotic

2. Kill bacteria = bactericidal antibiotic

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18
Q

What is the MIC?

A

Minimum inhibitory concentration = lowest concentration of drug needed to prevent growth

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19
Q

What is the MBC?

A

Minimum bactericidal concentration = lowest concentration that kills 99.9% of population

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20
Q

How is the MIC measured?

A

By tube dilution assay:

  1. Take a series of tube and dilute the drug serially
  2. Add bacteria to each tube and incubate them
  3. Test tube with minimum amount of drug and no bacterial growth is the MIC
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21
Q

How is the MBC measured?

A

Do tube dilution assay and then use a spread plate with correct tube to see if the bacterial were killed or simply prevented from growing

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22
Q

What is a disk diffusion assay? Other name?

A

Test for antibiotic sensitivity: take a large petri plate with disks impregnated with a different antibiotic on which bacteria is placed => the zones are then measured to tell whether the bacteria is sensitive

= Kirby-Bauer method

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23
Q

How to know if an antibiotic can be used clinically? What can be said if not?

A

Need to be able to achieve the MIC (preferably much higher than the MIC) within the bloodstream, urine, or site where the infection lies

If this is not achievable, then the bacteria is said to be clinically resistant

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24
Q

What is an E-test?

A

Test for antibiotic sensitivity: strips with varying concentrations of the antibiotic forming an elliptical zone of bacterial inhibition that intercepts the strip at the MIC

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25
Q

What is an antibiotic spectrum?

A

Range of bacteria species susceptible to the antibiotic

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26
Q

What 3 factors contribute to the antibiotic spectrum being narrow or broad?

A
  1. Target access
  2. Target affinity
  3. Susceptibility to inactivation
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27
Q

What are the 5 major mechanistic classes of antibiotics?

A
  1. Inhibitors of cell wall biosynthesis
  2. Inhibitors of protein biosynthesis
  3. Inhibitors of nucleic acid synthesis
  4. Metabolic Inhibitors
  5. Membrane disrupting agents
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28
Q

Other name for peptidoglycan bacterial cell wall?

A

Murein layer

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29
Q

How do β-lactam antibiotics work? 2 mechanisms.

A
  1. Inhibits cross-linking by binding the aminopeptidase penicilin binding protein in peptidoglycan bacterial cell wall synthesis
  2. Activate cell wall degradation enzymes, which the bacteria themselves are able to express under certain normal conditions to allow them to grow in a regulated manner => causes osmolysis
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30
Q

2 classes of antibiotics that are inhibitors of cell wall biosynthesis? Which is a bigger and more clinically relevant class?

A
  1. β-lactam antibiotics***

2. Non-β-lactam antibiotics

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31
Q

List 4 β-lactam antibiotics.

A
  1. Penicillins
  2. Cephalosporins
  3. Monbactams
  4. Carbapenems
32
Q

List 4 non-β-lactam antibiotics.

A
  1. Vancomycin
  2. Cycloserine
  3. Bacitracin
  4. Fosfomycin
33
Q

Why do antibiotics that are inhibitors of cell wall biosynthesis work?

A

Because mammalian cells do not have cell walls so they have very low toxicity

34
Q

Describe the core structure of β-lactam antibiotics. What to note?

A

4-C ring structure = cyclic amide cycled on the β-carbon

NOTE: 3D structure looks a lot like a peptide bond, which is why the penicillin binding protein can bind because it looks like the peptides it is trying to cross-link

35
Q

How do penicillins differ from each other?

A

Side chains

36
Q

What is an issue with the clinical application of penicillin G? Solution?

A

Cannot be taken orally as the stomach acid would hydrolyze the side chain

Penicillin V was invented instead

37
Q

Against what type of bacteria do penicillins work best?

A

Gram (+) bacteria

38
Q

What were a lot of the modifications made to penicillins geared at?

A

The drugs working against gram (-) bacteria

39
Q

4 subtypes of penicillins?

A
  1. Penicillin G
  2. Penicillin V
  3. Ampicillin
  4. Piperacillin
40
Q

What are the different types of cephalosporins?

A

Different generations of cephalosporins to enhance their effectiveness against gram (-) bacteria and other enhancements (e.g. being able to cross the BBB)

41
Q

How can bacteria become resistant to β-lactam antibiotics? How can this be dealt with? What to note?

A

When they express β-lactamases, enzymes that hydrolyze the lactam ring and destroy activity of the drug

Solution: β-lactamase inhibitors are used in combination with β-lactam antibiotics to prevent hydrolysis and destruction of the antibiotic (e.g. clavulanic acid and sulbactam, or augmentin = amoxicillin + clavulanic acid)

NOTE: number of β-lactamases is fast increasing and new one, New Delhi metallo-β-lactamase (NDM-1), now capable of cleaving carbapenems (e.g. against Klebsiella pneumoniae)

42
Q

How to recognize derivates of penicillin?

A

Suffix -cillin

43
Q

Are β-lactam antibiotics bacteriostatic or bactericidal antibiotics?

A

Bactericidal

44
Q

Caveat to β-lactam antibiotics working?

A

The bacteria need to be growing, i.e. they need to be in the right environment to be able to grow

45
Q

How do antibiotics hat are inhibitors of cell wall biosynthesis work against mycobacteria?

A

Unique inhibitors due to their unique cell wall:

  1. Ethambutol to inhibit synthesis of unique wall glycans
  2. Isoniazid inhibits the formation of mycolic acids
46
Q

7 types of antibiotics that inhibit protein biosynthesis?

A
  1. All 5 streptomyces antibiotics

6. Oxazolidinones

47
Q

4 aminoglycosides?

A
  1. Streptomycin
  2. Neomycin
  3. Kanamycin
  4. Gentamicin
48
Q

2 tetracyclines?

A
  1. Tetracycline

2. Doxycycline

49
Q

2 macrolides?

A
  1. Erythromycin

2. Azithromycin

50
Q

1 lincosamide?

A

Clarithromycin

51
Q

1 oxazolidinones?

52
Q

Why do antibiotics that inhibit protein synthesis work? What to note?

A

The structure of bacterial ribosomes differs from mammalian (cytoplasmic) ribosomes and the drugs inhibit either the initiation of protein synthesis or transpeptidation/translocation of the ribosome along the mRNA

Note: mitochondria have evolved from bacterial and the mitochondrial ribosome is more similar to bacterial ribosomes so some of these drugs could inhibit them

53
Q

3 types of antibiotics that inhibit nucleic acid synthesis?

A
  1. Rifamycins
  2. Quinolones
  3. Metronidazole
54
Q

4 rifamycins?

A
  1. Rifampin
  2. Rifabutin
  3. Rifaximin
  4. Rifapentine
55
Q

3 quinolones?

A
  1. Ciprofloxacin
  2. Levofloxacin
  3. Moxifloxacin
56
Q

How do rifamycins works?

A

They inhibit RNA polymerase, i.e. they inhibit RNA synthesis by binding to its β-subunit to inhibit mRNA synthesis

57
Q

How do quinolones work?

A

They inhibit topoisomerases (gyrase and topoisomerase IV) by binding to them and inhibiting them from unwinding DNA for replication

58
Q

How does metronidazole work? What to note?

A

Causes DNA cleavage

NOTE: drug specific against anaerobes

59
Q

2 types of antibiotics that are metabolic inhibitors? What to note?

A
  1. Sulfonamides
  2. Trimethoprim

NOTE: usually used together as it is easy to get mutations in these enzymes that will allow them to avoid binding the drug analogs

60
Q

Why do antibiotics that are metabolic inhibitors work?

A
  1. Enzymes unique to microbe

OR

  1. Structural difference between enzymes of bacteria and mammalian cells => drugs have MUCH higher affinity to the bacterial enzymes
61
Q

How do sulfonamides work?

A

Inhibit a step in the synthesis of folic acid, which bacteria synthesize de novo (which humans do not) because they are an analog of para-aminobenzoic acid which is involved in the formation of the folic acid precursor, dihydropteroic acid

62
Q

How does trimethoprim work?

A

Inhibits a subsequent step in the bacterial synthesis of folic acid during which dihydrofolic acid (DHFA) is reduced to tetrahydrofolic acid (THFA)

63
Q

What do bacteria use folic acid for?

A

Important for the synthesis of nucleic acids

64
Q

2 types of antibiotics that are membrane disrupting agents?

A
  1. Colistin = polymyxin

2. Daptomycin

65
Q

How does colistin work?

A

Binds lipid A of LPS

66
Q

How does daptomycin work?

A

Takes advantage of differences in membrane lipid composition

67
Q

How do antibiotics that are membrane disrupting agents work?

A

Form a pore in the membrane out of which cellular contents leak out

68
Q

2 important variables governing antibiotic use?

A
  1. Host-drug interactions

2. Microbe-drug interactions

69
Q

What are 3 examples of host-drug interactions?

A
  1. Pharmacodynamics: absorption => metabolism => excretion and whether or not the MIC will be reached
  2. Side effects
  3. Therapeutic index: toxic dose/therapeutic dose
70
Q

4 examples of antibiotic side effects?

A
  1. Hypersensitivity
  2. Tetracycline: tooth discoloration (due to binding with calcium)
  3. Quinolones: damage developing cartilage
  4. Aminoglycosides: 8th cranial nerve toxicity => deafness or loss of balance
71
Q

4 examples of microbe-drug interactions?

A
  1. Efficacious concentration
  2. Effect on microbe
  3. Spectrum
  4. Resistance
72
Q

Why does antimicrobial resistance occur?

A

Because the multiplication of resistant microbes is favored by presence of antibiotics (natural selection/survival of the fittest) => resistance is driven by human use and misuse of antimicrobials

73
Q

How can we prevent antimicrobial resistance?

A
  1. Reducing antimicrobial selection pressure

1. Preserving the utility of available drugs for as long as possible

74
Q

2 origins of antibiotic resistance genes in microbial pathogens?

A
  1. Spontaneous mutations
  2. Microorganisms in the environment = “Resistome”: made up of antibiotic producers and competitors of those AB producers (which evolve to combat them)
75
Q

4 mechanisms of dissemination of antibiotic resistance?

A
  1. Conjugative plasmids
  2. Transposons
  3. Transformation
  4. Transduction
76
Q

3 biochemical mechanisms of antibiotic resistance?

A
  1. Altered permeability: uptake or efflux
  2. Modified target: structure or amount
  3. Drug modification: hydrolyze or derivatize
77
Q

CDC key prevention strategies to prevent antimicrobial resistance?

A
  1. Prevent infection
  2. Diagnose and treat infection effectively
  3. Use antimicrobials wisely
  4. Prevent transmission

SMP - MIM Part 2 (13 decks)

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