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Infection and immunity > Antimicrobial modes of action > Flashcards

Antimicrobial modes of action Flashcards

1
Q

Name the three desirable properties of an antimicrobial.

A
  1. selective activity
  2. Cidal activity
  3. Slow emergency of resistance
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2
Q

What are the four possible modes of action of antibiotics?

A
  1. Cell wall
  2. Protein synthesis
  3. Cell membrane
  4. Nucleic acid synthesis
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3
Q

Why is inhibiting cell wall peptidoglycan synthesis an attractive MOA for antibiotics?

A

Mammalian cells do not posses a cell wall and contain no other macromolecules resembling peptidoglycan. Consequently, antibiotics which interfer with the synthesis and assembly of peptidoglycan show excellent selective toxicity.

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4
Q

What is the MOA of B lactams?

A

Inhibitors of cell wall synthesis.

1) Bind Penicillin bindings proteins (PBPs)
2) mimic d-ala d-ala residues on peptide side chain
3) stimulate autolysins - break down cell wall

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5
Q

What is the difference between gram negative and positive bacteria?

A

Gram negative - thin peptidoglycan wall, cell membrane present

Gram positive - thick wall, no cell membrane

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6
Q

What is the MOA of glycopeptides?

A

Inhibitors of cell wall synthesis

  1. Bind terminal D-ala, D-ala on peptide side chain. This prevents transglycolyse enzyme from adding PG monomer onto glycan chain
  2. Prevents X-linking
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7
Q

What class of antibiotic is vancomycin?

A

Glycopeptide

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8
Q

What class of antibiotic is teicoplanin?

A

Glycopeptide

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9
Q

What is the MOA of polymixins?

A

Act at cell membrane.
Disrupts membrane leading to leakage of cytoplasmic contents.
Binds tightly to lipid A component of LPS in the outer membrane of gram negative bacteria.

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10
Q

What is the MOA of ciprofloxacin?

A

Inhibit topoisomerase I and IV (inhibit DNA replication)

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11
Q

What does topoisomerase II (DNA gyrase) do?

A

Topoisomerase II is responsible for introducing negative supercoils into DNA and for relieving torsional stress, which accumalates ahead of site of transcription and replication.

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12
Q

What does topoisomerase IV do?

A

Topoisomerase IV provides a potent decatenating (unlinking activity) that removes links and knots generated behind the replication - separating DNA after replication.

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13
Q

Macrolides, streptogramins, lincosamides have overlapping binding sites - what is this?

A

Inhibitors of protein synthesis - act on the 50S ribosome.

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14
Q

What is the site of action of tetracyclines?

A

30S ribosome

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15
Q

What is the site of action of aminoglycosides?

A

30S ribosome

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16
Q

Outline the process of protein synthesis.

A
  1. Initiation
    - fmet-tRNA brought to AUG start codon (P site)
    - 30s subunit attaches to mRNA
    - 50s subunit completes initiation complex
  2. Elongation
    - 2nd tRNA enters A site
    - peptide bond between 1st and 2nd AA forms
    - translocation and release of tRNA (2nd tRNA enters P site, 3rd tRNA enters A site)
  3. Termination
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17
Q

What class of antibiotic is gentamicin?

A

Gentamicin

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18
Q

What class of antibiotic is Linezolid?

A

Oxazolidinones

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19
Q

What is the MOA of aminoglycosides?

A

Most AG bind to 30S ribosome subunit

  • this inhibits assembly of ribosome
  • decreased binding of tRNA and translocation

Some AGs bind to 50s ribosome subunit.

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20
Q

What is the MOA of oxazolidiones?

A

Bind 50s subunit - this inhibits assembly of initiation complex.

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21
Q

What class of antibiotic is doxycycline?

A

Tetracycline

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22
Q

What class of antibiotic is minocycline?

A

Tetracycline

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23
Q

What is the MOA of tetracyclines?

A

Binds to 30S ribosome - leads to decreased binding of tRNA to A site.

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24
Q

What is the MOA of chloramphenicol?

A

Binds to 50S subunit - decreased peptide bond formation.

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25
Q

What class of antibiotic is erythromycin?

A

Macrolide

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26
Q

What class of antibiotic is clarithromycin?

A

Macrolide

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27
Q

What is the MOA of macrolides?

A

Binds to 50S subunit - decreases translocation and release of tRNA.

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28
Q

What is the MOA of Fusidic acid?

A

Binds to EF-G ribosome complex?

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29
Q

Oral vancomycin is used for what?

A

C.diff

30
Q

what is the MOA of cycloserine?

A

Inhibits cell wall synthesis

31
Q

What infection is cycloserine used for?

A

TB

32
Q

What is the MOA of Bacitracin?

A

Inhibits cell wall synthesis

33
Q

What is polyfax (polymixin B and bacitracin) used to treat?

A

Used topically for skin and eye infections. Or for the preventions of wound infection.

34
Q

What is a common side effect of polyfax?

A

Contact dermatitis

35
Q

What is the MOA of polymixins?

A

affect cell membrane

36
Q

What class of antibiotic is daptomycin?

A

Lipopeptides

37
Q

What is the MOA of lipopeptides e.g. daptomycin?

A

Affect cell membrane by rapid depolarisation of cytoplasmic membrane leading to loss of function

38
Q

What is daptomycin used for?

A

Skin and soft tissue infections (SSTIs), endocarditis

39
Q

What enzyme does trimethoprim inhibit?

A

Dihydrofolate reductase

40
Q

What enzyme does sulphonamide inhibit?

A

Dihydropterate synthetase

41
Q

What is the main use of oral trimethoprim?

A

Gram -ive UIT (e.g. e.coli)

42
Q

Co-trixamole is used to treat what?

A

Pneumoncystis pneumonia (PCP)

43
Q

What is the MOA of fluroquinolones?

A

inhibitors of DNA replication. Inhibits DNA gyrase and Type IV topoisomerase

44
Q

What class of antibiotic is ciprofloxacin?

A

Fluoroquinolone

45
Q

Is ciprofloxacin bacteriostatic or cidal?

A

Bactericidal

46
Q

Ciprofloxacin has low oral BA….true/false?

A

False - oral BA 70-85%

47
Q

what are the uses of ciprofloxacin?

A

Active against gram -ive bacteria
Intracellular pathogens - chlamydia
RIT, UTI, GIT

48
Q

Rifamycins are inhibitors of what?

A

Inhibitors of RNA polymerase

49
Q

Rifampicin is used for what?

A

Orally for TB and prophylactically against meningitis of infections of prosthetic material

50
Q

Why is gentamicin not used for infections caused by anaerobic bacteria?

A

Uptake is dependent on energy derived from aerobic metabolism.

51
Q

Why is gentamicin not used for intracellular infections?

A

Poor ability to penetrate the eukaryotic cell membrane

52
Q

Why is once daily dosing possible with gentamicin?

A

Long post antibiotic effect (PAE)

53
Q

True or false. Amino glycosides are used to treat meningitis

A

False - poor penetration into the CSF.

54
Q

Why are Amino glycosides nephrotoxic?

A

Small portion of the dose is retained in the epithelial cells lining the S1 and S2 segments of the proximal tubules.

55
Q

What is the MOA of tetracyclines?

A

Bind 30S subunit, decrease tRNA binding to A site. Irreversible of binding.

56
Q

What can affect the absorption of tetracyclines?

A

Iron, antacids, dairy. Chelation and changes in pH

57
Q

What are the side effects of tetracyclines?

A

Mainly GI, deposition in bones/teeth, headache, kidney/liver damage, phototoxicity.

58
Q

What is the alternative medication to penicillins for a patient who has Strep. throat but has a penicillin allergy?

A

Erythromycin/clarithromycin

59
Q

What is the MOA of clindamycin?

A

Protein synthesis - overalapping site of ribsosome

60
Q

True/False: Fusidic acid has a narrow spectrum.

A

True

61
Q

What medicines should be used with caution alongisde Oxalidiones such as Linezolid, and why?

A

Weak MAO inhibitor - can’t take with tyramine rich foods, caution with antidepressants and opiates.

62
Q

What is the very severe side affect associated with oral chloramphenicol?

A

Risk of fatal aplastic anaemia

63
Q

Name four causes of TB

A

M. tuberculosis.
M. Boris.
M. Africanum.
Mi. Microti

64
Q

Outline the stages of primary TB progression.

A
  1. bacilli inhalation and phagocytosis by macrophages (does not destroy bacillus)
  2. TB multiplies insides macrophage for 7-21 days until marophage bursts
  3. incoming macrophages phagocytose released TB
  4. cell mediated response initated and tubercules formed
  5. bacteria multiply inside macrophages, uncontrolled lysis
  6. enzymes released destroy local tissue
65
Q

How do we diagnosis ACTIVE tb?

A

Clinical examination
Chest X-ray - look for white lesions
Sputum test/smears/culutres - staining and microscopy

66
Q

How do we diagnose latent TB?

A

Tuberculin skin test - s/c injection. postive result = skin lesion >10mm diameter after 48-72 hours.

or

Molecular assays

  • Xpert MTB/RIF assay
  • interferon gamma tests
67
Q

What are the four 1st line drugs for TB?

A
  1. Rifampicin
  2. Isonialoid
    3, Pyrazinamine
  3. Ethambutol
68
Q

What are the six 2nd line drugs for TB?

A 
streptomycin
capreomycin
cyclosterine
ciprofloxacin
azithroymycine
69
Q

How do we treat active tb?

A

Rifampicin and isonizaoid for 6-9months

OR

pyrazinamide for 2 months and ethambutol

70
Q

How do we treat latent tb?

A

Isoniazid for 6 months
or

rifampicin and isoniazid (3 months)

Infection and immunity (13 decks)

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