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BMS662: MICROBIAL PATHOGEN > C7 > Flashcards

C7 Flashcards

1
Q

Types of antimicrobial drugs

A
  • Synthetic: salvarsan & sulpha
  • Natural: penicillin
  • Semi synthetic: semi synthetic penicillin
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2
Q

General properties of antimicrobial drugs

A

Selective toxicity
- Drug able to kill or inhibit organism without causing damage to host

Spectrum of activity
- Range of different microbes against antimicrobial agent

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3
Q

Modes of action of antimicrobial drugs

A
  • Antibacterial
  • Antiviral
  • Antifungal
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4
Q

Spectrum of antibacterial drug

A
  • Broad spectrum agent
  • Narrow spectrum agent
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5
Q

2 category of anti bacterial drugs

A
  • Bactericidal agent: kill
  • Bacteriostatic agent: stunt growth
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6
Q

Mechanism of action of antibacterial agents

A
  • Inhibition of cell wall synthesis: Penicillin
  • Disruption of cell membrane function: Polymyxin
  • Inhibition of protein synthesis: Tetracycline
  • Inhibition of nucleic acid synthesis: Rifamycin
  • Action as metabolites: Sulfonamides & Trimethoprim
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7
Q

Example of cell wall inhibitors

A
  • Beta lactam
  • Penicillin
  • Cephalosporin
  • Penem antibiotic
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8
Q

Mechanism of penicillins in cell wall synthesis

A
  • Cell wall synthesis catalyst by transpeptidase
  • Penicillin bind to transpeptidase & inhibit cross linking
  • Newly synthesis cell wall no longer cross linked & not strong
  • Induce autolysin that digest existing cell wall to cause cell lysis
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9
Q

Mechanism in semi synthetic penicillin

A
  • Made by changing the R side chain on Penicillin G molecule
  • Acid stable & resistant beta lactamase
  • Eg: ampicillin & methicillin
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10
Q

Explain cephalosporin

A
  • Produce by Cephalosporium
  • More resistant to beta lactamase
  • Use to combat Neiserria
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11
Q

Explain bacitracin & vancomycin

A

Bacitracin
- Small polypeptide produce by B.lichenoformis
- Inhibit symptoms of peptidoglycan strand
- Use topically

Vancomycin
- Quite toxic
- Use as last line defence

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12
Q

Explain mechanism of cell membrane disruptor

A
  • 5 types of polymyxins (A,B,C,D &E)
  • Binding to lipid in outer membrane
  • Tyrocidins similar to polymyxin & toxic
  • Daptomycin bind to bacterial cytoplasmic membrane, form pore & induce depolarisation
  • Cell lose ability to synthesis proteins & nucleic acid results in cell death
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13
Q

Explain mechanism antibiotic affecting protein synthesis

A
  • Inhibit protein synthesis on bacterial ribosome
  • Bacteria has 70S ribosome consist of 50S & 30S
  • Eukaryotic has 80S ribosome consist of 60S & 40S
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14
Q

Inhibitor 30S ribosomal unit

A

Aminoglycosides
- Bind irreversibly to 30S
- Stop initiation complex
- Seldom use due to resistance
- Can act synergistically with other drugs

Tetracycline
- Inhibit binding of aminoacyl tRNA to acceptor
- Widest spectrum
- Destroy normal intestinal microflora

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15
Q

Inhibitor of 50S ribosomal unit

A

Erythromycin
- Bind to 23SRNA of 50S
- Inhibit function of peptidyl tRNA
- Macrolide ring structure with sugars

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16
Q

Inhibitor of nucleic acid synthesis

A

Quinolones
- Inhibit enzyme DNA gyrase
- DNA gyrase catalyst supercoiling of DNA
- Prevent DNA synthesis

Rifampin/ Rifamycin
- Block DNA dependent RNA polymerase enzymes
- Inhibit intiation of RNA transcription
- Treat TB

17
Q

Example of antimetabolite

A
  • Sulfonamides
  • Trimethoprim
18
Q

Explain sulfonamides & trimethoprim

A

Sulfonamides
- Growth factor analogs
- Block use of growth factor by competing same enzyme
- Bind to PABA & bacteria stop grow w/o folic acid

Trimethoprim
- Bind to dihydrofolate reductase & inhibit formation of tetrahydrofolic acid
- Use in combination with sulfonamides
- Prevent emergence of resistant strain

19
Q

Why fungi difficult to treat

A
  • Difficult to find target unique to fungal cell
  • Drug inhibit metabolic pathways also effect human cell
  • Most drug are toxic & topical application only
20
Q

Antifungal drug mechanism

A
  • Membrane function: Polyenes
  • Nucleic acid synthesis: 5-Fluorocytosine
  • Microtubules formation: Griseofulvin
  • Ergosterol synthesis: Azoles
  • Cell wall synthesis: Polyoxins
21
Q

Explain membrane function disruptor in antifungal drug

A
  • Bind to ergosterol in fungal cell membrane
  • Cause membrane permeability & cell death
  • Azoles & allylamides inhibit ergosterol synthesis
  • Broad spectrum
22
Q

Explain inhibitor of cell wall synthesis in antifungal drug

A
  • Polyoxin interfere with chitin synthesis
  • Cell wall also contain glucan polymer synthesis by enzymes 1,3 b-D glucan synthase
23
Q

Example of inhibitors of nucleic acid synthesis

A
  • Nucleotide analog
  • Eg: 5-fluorocytosine
  • Effective inhibitors of nucleic acid synthesis
24
Q

Explain disruption of microtubule formation

A
  • Griseofulvin disrupt microtubule assembly during mitosis
  • Cell cannot divide
  • Useful as anticancer drug
  • Expensive cuz source difficult to find
25
Q

Drug use to target virus entry

A
  • Enfuvirtide
  • Amantadine & Rimantadine
26
Q

Drug use in virus genome replication

A
  • Ayclovir
  • Ganciclovir
  • Foscarnet
27
Q

Explain acylovir, ganciclovir & foscarnet

A

Acylovir
- Need to be phosphorylated before inhibit DNA polymerase
- Blocking further elongation in DNA replication

Ganciclovir
- Similar mechanism to acylovir
- More toxic
- Reduce amount of CMV

Foscarnet
- Directly inhibit enzymatic activity of herpesvirus DNA polymerase

28
Q

Example of nuclease inhibitor in HIV & HBV

A

Zidovudine (ZDV/ AZT) or nucleoside transcriptase inhibitors (NRTI)

29
Q

Explain ZDV

A
  • First anti HIV drug
  • Analog of thymidine
  • Inhibit the HIV & prevent elongation of viral nucleic acid
30
Q

Explain nonnucleoside inhibitors of HIV RT

A
  • Include delavirdine, efavirenz & nevirapine
  • Inhibit HIV reverse transcriptase
  • Inhibit catalytic step in RT by binding directly to reverse transcriptase & inactivating enzyme
31
Q

Mechanism of neuramidase (NA) inhibitors

A
  • Inhibit virus release from infected cell
  • Removal of sialic acid vital for release of virus from infected cell & spread effectively
  • Absence of NA cleavage or terminal sialic acid, virus aggregate as it release & cannot spread efficiently
  • Eg NA inhibitor is tamiflu
32
Q

Explain interferons

A
  • Small protein that prevent viral multiplication by stimulating production of antiviral protein
  • Natural molecules
  • 3 types: IFN-a, IFN-y & IFN-B
  • Host specific activities
33
Q

Why interferon fail to provide broad spectrum antiviral activity

A
  • Production of interferon different in response to different virus, thus its not effective
  • Active against RNA virus only which do not cause disease and not DNA
34
Q

Explain prophylaxis vaccine

A
  • Introduce antigen to body
  • Goal to induce immune system to create antibodies for antigen hence become immune to the illness
  • Encourage body to fight harder against illness it already has
35
Q

Types of immunisation

A

Passive
- Acquire from maternal antibodies, antitoxin
- Temporary

Active
- Acquire from natural infections, vaccine & toxoid
- Permanent

BMS662: MICROBIAL PATHOGEN (7 decks)

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