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L15

Terms in this set (12)

Antimicrobial
Any kind of microbial that can heal a virus, microbe, bacteria or protist
-They have to be selectively toxic. i.e. kills microbes without killing human host
Antibiotic
A natural microbial product that acts to kill bacteria
Therapeutic index
Toxic dose (Max conc.)/Therapeutic dose (Min conc.)
Bacteriostatic, Bactericidal, Bacteriolytic
-Bacteriostatic: stops growth but doesn't kill cell (reversible)
-Bactericidal: Stops growth and kills cells (irreversible)
-Bacteriolytic: stops growth and kills and lyses cells (Irreversible)
Bacteriolytic (e.g. penicillin)
Type of inhibition:
-Inhibitors of cell wall synthesis

Mechanism of action:
-They attack the synthesis of the cell wall, not peptidoglycan and stop the cells form making new peptidoglycan.
-It acts as a substrate analogue. i.e. it binds to the active site of the enzyme because they have a similar shape to the normal substrate of the enzyme

Typical target bacteria:
-Penicillin bind to transpeptidase enzyme, preventing Alanyl-alanine from binding to the active site

Mechanisms of resistance:
-Beta lactamase breaks B-lactam ring, making it chemically inactive. i.e. penicillin no longer binds to the active site and is not working
-Beta lactamase resistance genes are widespread in G+ve and G-ve's carried by tansporsons
Bacteriolytic (e.g. Cephalosporins)
Type of inhibition:
-Inhibitors of cell wall synthesis

Mechanism of action:
-They attack the synthesis of the cell wall, not peptidoglycan and stop the cells form making new peptidoglycan.
-It acts as a substrate analogue. i.e. it binds to the active site of the enzyme because they have a similar shape to the normal substrate of the enzyme

Typical target bacteria:
-Work best on G+ve bacteria
-Binds to transpeptidase enzyme, preventing Alanyl-alanine from binding to the active site
Bacteriolytic (Vancomycin comes from Amycolatopsis because of its complicated structure and cannot be replicated manually)
Type of inhibition:
-Inhibitors of cell wall synthesis

Mechanism of action:
-They attack the synthesis of the cell wall, not peptidoglycan and stop the cells form making new peptidoglycan.
-It acts as a substrate analogue. i.e. it binds to the active site of the enzyme because they have a similar shape to the normal substrate of the enzyme

Typical target bacteria:
-Work best on G+ve bacteria

Resistance
-Very few are resistant to this, but this med is used as alast resort so its not good that there are some microbes resistant to it
Bactericidal ( Streptomycin)
Type of inhibition:
-Inhibitors of protein synthesis

Mechanism of action:
-They attack ribosomes
-They block up the ribosome, so the cell can't make protein. If they can't make protein then that causes the cell to die

Target Bacteria:
-G+ve

Resistance:
-Enzyme activity in the bacteria, add bits on to the structure of the antimicrobe, which stops the antimicrobial from binding the target site. This is known as acquired resistance
-Spontaneous Chromosomal Mutation which changes the structure of the ribsomeon where strep cannot bid to the ribosome
-broad spectrum resistance i.e. more types of mycins have resistances
Bacteriostatic ( Tetracycline)
Type of inhibition:
-Inhibitors of protein synthesis

Mechanism of action:
-They attack ribosomes
-They block tRNA frombinding to the ribosome and this means that it stops the cells form temporarily growing
-They have a low therapeutic index and dangerous for pregnant women

Target Bacteria:
- G+ve and G -ve
-For bacteria that don't have a cell wall

Resistance:
1. Some bacteria have efflux pumps which pump out the tetra from the cell. Predominantly found in G-ve
2. Have ribosome protective sites that block binding of tetra to active sight. PRedominantly found in G+ve
Bacteriostatic (Sulfonamides)
Type of inhibition:
-Block metabolic pathways

Mechanism of action:
-inhibits folic acid synthesis
-Blocking synthesis of this vitamin causing the cell to stop growing

Target Bacteria:
- Structural analogs of PABA

Resistance:
1. Spontaneous mutations that can change the enzyme so the drugs no longer bind to the active site
2. Acquired, which alters enzyme
Antifungal agents (Sterols)
- Fungi have diff sterols to humans
-By inhibiting this pathway we can kill the fungi
i.e. ketoconazole
Antiviral Agents
-The viruses are different to us and very tiny and small genome so hard to find antivirals due to host toxicity
-Most antivirals target DNA polymerase of the virus, by inhibiting this it will kill the virus because it can no longer replicate
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