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BSCI 2150 > Week 14.1 Antimicrobials > Flashcards

Week 14.1 Antimicrobials Flashcards

1
Q

What things are used to to kill bacteria or inhibit their growth?

A

antibiotics and disinfectants

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2
Q

Examples of antibiotics and disinfectants

A

-Penicillin prevents bacteria from building a cell wall (block peptidoglycan)
-Chloramphenicol and tetracycline inhibit protein synthesis
-Rifampicin inhibits RNA transcription
-Alcohol dissolves bacterial membrane

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3
Q

Why don’t antibiotics or disinfectants kill us like they do bacteria?

A

We have slight structure differences in ribosomes so they don’t target our cells

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4
Q

Antibiotics bind to…

A

proteins

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5
Q

Competitive inhibition vs noncompetitive inhibition

A

-Competitive: competitive inhibitor and substrate compete for active site
-Noncompetitive: competitive inhibitor binds to allosteric site that induces a conformational change in the active site, preventing the substrate from binding to it

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6
Q

Bacteriostatic

A

the growth of the bacteria is inhibited but the bacteria are not necessarily killed

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7
Q

Bactericidal

A

the bacteria are killed

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8
Q

Six primary antibiotic targets in bacteria

A
  1. Cell membrane
  2. Cell wall synthesis
  3. DNA replication
  4. RNA synthesis
  5. Protein synthesis
  6. Metabolism (folic acid synthesis)
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9
Q

Other special antibiotic targets in bacteria

A
  1. Biofilm formation
  2. Flagella/pilli
  3. Quorum sensing
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10
Q

What do you need to know to predict how an antibiotic will affect a cell?

A
  1. Antibiotic’s target
  2. Target’s function
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11
Q

What is the bacterial plasma membrane?

A

A phospholipid bilayer with a variety of embedded proteins, lipids, and carbohydrates that perform various functions for the cell

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12
Q

Functions of embedded proteins

A
  1. Transport
  2. Enzymatic activity
  3. Signal transduction
  4. Cell-cell recognition
  5. Intracellular joining
  6. Attachment to the cytoskeleton and ECM
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13
Q

Antibiotics that disrupt the bacterial membrane

A
  1. Daptomycin: causes depolarization of cytoplasmic membrane, resulting in disruption of ionic concentration gradients
  2. Bacitracin: inhibits export of peptidoglycan precursors
  3. Polymyxins: disrupts the membrane
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14
Q

Isotonic solution

A

no net movement of water particles; cell membrane is attached to cell wall

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15
Q

Hypertonic solution

A

water particles move OUT of the cell; cell membrane shrinks and detaches from cell wall (plasmolysis)

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16
Q

Hypotonic solution

A

water particles move INTO the cell; cell wall counteracts osmotic pressure to prevent swelling and lysis

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17
Q

Peptidoglycan

A

a polymer composed of alternating N-acetylmuramic acid (NAM) and N-acetylglucosamine (NAG)
-NAM: peptide sidechain
-NAG: does not have peptide sidechain

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18
Q

NAG-NAM synthesis

A
  1. NAM is synthesized in the cytoplasm and linked to UDP
  2. NAM is linked to bactoprenol
  3. NAG is added to NAM
  4. Bactoprenol flips NAM-NAG to periplasm
  5. Transpeptidase polymerizes the disaccharides into the growing peptidoglycan chain (crosslinking occurs)
  6. Bactoprenol flips back to cytoplasm
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19
Q

Why are peptide chains on 2 stacked N-acetylmuramic acids crosslinked?

A

to stabilize the layers

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20
Q

What is separation of bacterial daughter cells controlled by?

A

FtsZ protein

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21
Q

How do bacterial cells divide using FtsZ protein?

A

FtsZ proteins assembled along the membrane and form the Z ring. Then the Z ring is anchored to the membrane and pinches together to cleave the cells.

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22
Q

How do bacterial cells with cell walls divide?

A

Autolysins (an enzyme) cleave peptidoglycan so the dividing cell can separate
-Ex: amidase

23
Q

What happens when autolysins cleave the cell wall?

A

New peptidoglycan is inserted along the break to facilitate elongation and septum formation

24
Q

Antibiotics that affect cell wall synthesis

A
  1. Beta-lacams
  2. Beta-lacam/B-lactamase inhibitors
  3. Vancomycin
  4. Bacitracin
  5. Isoniazid/ethionamide
  6. Ethambutol
  7. Cycloserine
25
Q

Beta-lacams

A

-Penicillins, cephalosporins, cephamycins, carbapenems, monobactams
-Mechanism: Bind proteins and enzymes responsible for peptidoglycan synthesis

26
Q

Beta-lacam/beta-lactamase inhibitors

A

Bind beta-lactamases and prevent INactivation of lactam

27
Q

Vancomycin

A

Inhibits cross-linkage of peptidoglycan layers

28
Q

Bacitracin

A

Inhibits export of peptidoglycan precursors

29
Q

Isoniazid/ethionamide

A

Inhibit mycolic acid synthesis (mycobacterium)

30
Q

Ethambutol

A

Inhibits arabinogalactan synthesis (mycobacterium)

31
Q

Cycloserine

A

Inhibits cross-linkage of peptidoglycan layers

32
Q

Central Dogma of Molecular Biology

A

DNA > RNA > protein

33
Q

DNA replication (summarized)

A
  1. Complementary strands of DNA must be separated and prevented from rewinding (DNA gyrase, helicase, single-stranded binding proteins)
  2. DNA polymerase requires an RNA primer to bind to DNA (RNA primase)
  3. Discontinuous strands must be ligated together (Okazaki fragments and DNA ligase)
34
Q

DNA gyrase

A

relaxes supercoiling

35
Q

Helicase

A

separates strands of DNA

36
Q

Single-stranded binding proteins

A

prevent DNA from coming back together

37
Q

RNA primase

A

adds complementary RNA nucleotides to DNA
-allows attachment of DNA polymerase
-problem: RNA nucleotides instead of DNA

38
Q

Okazaki fragments

A

short sequences of DNA that are synthesized discontinuously

39
Q

DNA ligase

A

joins the 5’ phosphate to the 3’ end hydroxyl

40
Q

Antibiotics that disrupt DNA replication

A
  1. Quinolones
  2. Metronidazole
41
Q

Quinolones

A

-nalidixic acid, ciprofloxacin, levofloxacin, moxifloxacin
-Mechanism: inhibits DNA gyrase (strands remain extremely supercoiled)

42
Q

Metronidazole

A

Disrupts host DNA and therefore DNA replication

43
Q

RNA polymerase

A

able to bind DNA, unwind, unzip, and polymerize without help from other enzymes

44
Q

Antibiotics that disrupt RNA synthesis

A
  1. Rifampin (rifampicin): inhibits RNA polymerase
  2. Rifabutin: inhibits RNA polymerase
    *bacteriostatic
45
Q

Antibiotics that disrupt protein synthesis

A
  1. Aminoglycosides
  2. Tetracyclines
  3. Glycylclines
  4. Oxazolidinone
  5. Macrolides, ketolides, clindamycin, streptogramins
46
Q

Aminoglycosides

A

-streptomycin, kanamycin, gentamycin, tobramycin, amikacin
-Mechanism: produce premature release from 30S ribosomal subunit

47
Q

Tetracyclines

A

Prevent peptide elongation at 30S ribosomal subunit

48
Q

Glycyclines

A

Bind to 30S ribosomal subunit (prevent 50S from binding)

49
Q

Oxazolidinone

A

Prevents initiation of protein synthesis at 50S ribosomal subunit

50
Q

Macrolides, ketolides, clindamycin, streptogramins

A

Prevent polypeptide elongation at 50S ribosome

51
Q

Why is folic acid important for protein and nucleic acid synthesis?

A

It’s a required precursor

52
Q

Why is folic acid synthesis not a good target?

A

-bacterial cells can become persister cells
-bacterial cells can also get folic acid from nearby

53
Q

Antibiotics that disrupt folic acid synthesis (aka antimetabolites)

A
  1. Sulfonamides: inhibit dihydropteroate synthesis and disrupt folic acid synthesis
  2. Dapsone: inhibits dihydropteroate synthase
  3. Trimethoprim: inhibits dihydrofolate reductase and disrupts folic acid synthesis

BSCI 2150 (11 decks)

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