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A. BIOM3011 > Antibacterials > Flashcards

Antibacterials Flashcards

1
Q

Define bacteriostatic

A

Prevents growth and replication

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2
Q

Define bactericidal

A

Kills bacteria

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3
Q

Explain the differences between bacterial and eukaryote cell walls

A

Bacterial = rigid
Eukaryote = semi-permeable membrane

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4
Q

Name 3 mechanisms of acquiring resistance genes

A
  • conjugation
  • transduction
  • transformation
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5
Q

Explain the conjugation method of acquiring resistance genes

A

Where two bacteria exchange genetic information between themselves - can pass on resistance genes

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6
Q

Explain the transduction method of acquiring resistance genes

A

Genetic material is exchanged between bacteria using a virus (a phage - virus specific to bacteria)

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7
Q

Explain the transformation method of acquiring resistance genes

A

Bacteria pick up exogenous DNA from the environment

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8
Q

Bacterial cell wall is made up of what?

A

Peptidoglycan - a sugar backbone unique to bacteria

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9
Q

Transpeptidase is also known as?

A

Penicillin binding protein

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10
Q

MOA of B-lactam antibiotics?

A

They form a covalent bond with transpeptidase which interferes with the synthesis of the cell wall by preventing the cross linking of peptidoglycan chains that is facilitated by transpeptidase

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11
Q

Name 2 mechanisms for resistance for B-lactam antibiotics

A
  • enzymatic degradation - bacteria acquires a b-lactamase enzyme which degrades the drug
  • altered receptor - bacteria acquires a new version of transpeptidase which does not bind to drug
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12
Q

True or false: cephalosporins are fungi-derived

A

True

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13
Q

Is cefalexin susceptible to degradation by B-lactamase

A

Yes

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14
Q

Vancomycin MOA?

A

Interferes with cell wall synthesis. Binds to the end of the D-Ala-D-Ala sequence which prevents transpeptidase from binding and forming a cross link.

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15
Q

Mechanism for resistance against vancomycin?

A

Altered receptor = The bacteria can change the D-Ala-D-Ala into D-Ala-D-Lac. This prevents vancomycin from binding, however can still bind to transpeptidase
Example: VRE

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16
Q

Explain the cell wall of TB

A

TB is a mycobacterium. This means it’s cell wall is largely made up of mycolic acid. This specialised cell wall is what prevents the mycobacterium from being killed by macrophages

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17
Q

Isoniazid MOA and indication?

A

A TB drug
Prevents the synthesis of mycolic acid
I.e. interferes with cell wall synthesis

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18
Q

Isoniazid mechanism of resistance?

A

Isoniazid typically gets converted into active form by the mycobacterium catalase enzyme which is encoded by the katG gene. Mutations in this gene prevent the formation of this enzyme, preventing the activation of the drug

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19
Q

Explain what a granuloma is

A

A granuloma is a cluster of TB living inside immune cells. The TB is dormant in the granuloma

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20
Q

What could cause a granuloma to become active

A

If the patient becomes immunocompromised

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21
Q

Explain the MOA of rifampicin

A

Blocks RNA synthesis by inhibiting bacterial RNA polymerase - blocks transcription

By blocking RNA synthesis, you are preventing the formation of proteins essential for replication

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22
Q

Discuss the resistance for rifampicin

A

Develops rapidly.
A mutation in the gene that encodes for the RNA polymerase causes a change in the B subunit that the drug binds to.
Need to use rifampicin in combination therapy

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23
Q

Name 2 drugs that are folate synthesis inhibitors

A

Trimethoprim and a sulfonamide (like sulfamethoxazole)

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24
Q

Why would inhibiting folate synthesis be a good mechanism for anti bacterial drugs?

A

Because the folate is required for DNA and RNA synthesis in bacteria.
It is specific to bacteria because they synthesise their own folate, whereas humans get it from their diet

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25
Q

DHFR stands for?

A

Dihydrofolate reductase

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26
Q

MOA of sulfonamides?

A

Structural analog for PABA (p-aminobenzoic acid) which is a precursor to folic acid. Drug competes with PABA for binding to an enzyme. Reduces the production of folic acid

27
Q

MOA of trimethoprim?

A

A competitive antagonist for DHFR, which typically converts folic acid into dihydrofolate (more active form)

28
Q

How do sulfonamides and trimethoprim work synergistically?

A

Sulfonamides reduce the production of folic acid, meaning there is less folic acid for trimethoprim to compete with for binding to DHFR

29
Q

Explain how the bypass mechanism of resistance reduces efficacy of trimethoprim

A

The bacteria increases concentration (upregulates) of DHFR enzyme. More receptors available = less effective competitive antagonist

30
Q

Which drug class can cause SJS?

A

Sulfonamides

31
Q

Explain how some bacteria are instrinsically resistant to sulfonamides

A

They do not need PABA to make their folate

32
Q

Is isoniazid a prodrug?

A

Yes

33
Q

DNA gyrase is also known as?

A

Topoisomerase II

34
Q

Is topoisomerase IV more common in gram negative or positive bacteria?

A

Positive

35
Q

Which topoisomerase enzyme relieves concatenation?

A

IV

36
Q

Which enzyme relieves supercoiling?

A

Topoisomerase II

37
Q

Ciprofloxacin belongs to which class of drugs?

A

Fluoro-Quinolones

38
Q

Name a fluoroquinolone

A

Ciprofloxacin, norfloxacin

39
Q

MOA of fluoroquinolones?

A

Inhibits topoisomerase II and IV. Binds to the alpha and beta subunits of the enzymes to prevent them from re-sealing the DNA

40
Q

Action of topoisomerases?

A

They cut, then re-seal DNA strands when supercoiled or concatenated

41
Q

Name 1 resistance mechanism for the fluroquinolones

A

-mutation in alpha subunit reduces binding affinity
- a plasmid-encoded protein binds to topoisomerase and protects it
- norA gene is acquired which encodes for an efflux pump for the drug

42
Q

Which bacteria are intrinsically resistant to metronidazole and why?

A

Aerobic bacteria. This is because they lack the enzyme required to activate the drug

43
Q

MOA of metronidazole?

A

Once activated, the drug is chemically reactive and causes damage to the DNA. It damages the DNA faster than it can be repaired, leading to accumulation and cell death

44
Q

Role of the pyruvate:ferredoxin oxidase enzyme?

A

Responsible for converting metronidazole into its active form

45
Q

Discuss the reaction between metronidazole and alcohol

A

Metronidazole inhibits the aldehyde dehydrogenase enzyme - the enzyme responsible for breaking down alcohol.

46
Q

Mechanisms for resistance in metronidazole?

A
  • mutations in the pyruvate:ferredoxin oxidase enzyme (needs this enzyme to be activated)
  • over expression of the gene (RecA) that encodes the protein responsible for DNA repair
47
Q

Name 3 classes of protein synthesis inhibitors

A

Aminoglycosides, macrolides, tetracyclines

(MAT)

48
Q

Which class does gentamicin belong to?

A

Aminoglycoside

49
Q

Why is gentamicin more effective on aerobic bacteria?

A

It’s uptake is oxygen dependent

50
Q

Which class of drugs are cationic?

A

Aminoglycosides

51
Q

What effect do cationic drugs have on bacteria?

A

They bind to the anionic bacteria membrane and disrupt it. This allows leakage of intracellular contents and increased drug uptake through the pores

52
Q

Gentamicin can be combined with which drugs for a synergistic effect?

A

Cell wall drugs (like b-lactams)
Due to cationic effect

53
Q

MOA of aminoglycosides?

A

Bind to the 30S subunit and prevent elongation step of protein synthesis. Also causes misreading of mRNA - causing abnormal protein production

54
Q

Resistance mechanism for gentamicin?

A
  • alteration to 30S subunit to prevent binding
  • acquisition of an enzyme that can degrade the drug
55
Q

Name a macrolide

A

Erythromycin or clarithromycin

56
Q

Name a lincosamide

A

Clindamycin

57
Q

MOA of macrolides?

A

Bind to the 50S subunit of the ribosome and prevent translocation step of protein synthesis

58
Q

Resistance mechanism for macrolides?

A
  • alteration to 50S subunit
  • acquisition of an enzyme that degrades the drug
  • increased expression of efflux pumps
59
Q

Name 2 tetracyclines

A

Tetracycline and doxycycline

60
Q

MOA of tetracyclines?

A

Binds to 30S subunit of ribosome and prevents tRNA from binding which blocks protein synthesis

61
Q

Why do tetracyclines cause issues with bones and teeth?

A

They bind to calcium

62
Q

MOA of mupirocin?

A

Prevents the amino acid isoleucyl from joining the growing protein chain. Causes production of the incorrect protein.

63
Q

Types of bacteria gentamicin is effective against?

A

Gram negative and aerobic (uptake into cell is oxygen dependent)

A. BIOM3011 (10 decks)

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