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Antibiotics Flashcards

1
Q

What do antibiotics do?

A

• Kill or inhibit the growth of other microorganisms to give the bacteria producing the antibiotic a selective advantage

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2
Q

What are most antibiotics derived from and then modified chemically to?

A

• Most derived from natural products by fermentation, then modified chemically to:
○ ≠ pharmacological properties
○ ≠ antimicrobial effect

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3
Q

What does antibiotics plus immunity give?

A

Gives bacterial clearance

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4
Q

What are the principles of antibiotics as therapeutic agents?

A
  1. Selective toxicity

2. Therapeutic margin

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5
Q

What is selective toxicity due to?

A

• Due to the differences in structure and metabolic pathways between host and pathogen

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6
Q

What is therapeutic margin?

A

• Active dose vs. toxic effect

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7
Q

What is a narrow therapeutic index?

A

margin between safe and harmful is small

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8
Q

What is a drug with a wide therapeutic margin?

A

If a drug is very safe and not very toxic

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9
Q

What is minimum inhibitory concentration?

A

concentration of drug needed to be effective

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10
Q

What can vancomycin cause?

A

toxic and can cause hearing damage in high doses

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11
Q

What do we need to make sure when giving antibiotics?

A

○ Need to make sure you give enough antibiotic to reach the MIC but also to not be toxic

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12
Q

What concept is microbacterial antagonism?

A

The concept that one organism can produce a substance that inhibits the growth of another

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13
Q

Where does microbacterial antagonism and why?

A

Happens in the gut as there is a large number of micro-organisms and they are able to co-exist

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14
Q

What do the microorganisms in the gut secrete and what do these secretions do and affect?

A

§ They secrete anti-microbial peptides and other compounds that limit growth of some organisms and prevent over-growth of others so they are able to co-exist

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15
Q

What can some antibiotics mess up and what can this cause?

A

• Some antibiotics completely mess up the homeostatic, commensal organisation of gut or skin flora
§ This can cause disease

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16
Q

When does clostridium difficile over grow microorganism and what is it associated with?

A

§ As the flora is disrupted, one of the microorganisms that overgrows is clostridium difficile
-Associated with diarrhoea outbreaks in hospital ICUs so serious hospital cross-infection risks due to easy spread of spores

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17
Q

What are antibiotics classified by?

A

○ Type of activity
○ Structure
○ Target site for activity

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18
Q

What are the 2 types of activities of antibiotics?

A
  1. Bacteriostatic

2. Bactericidal

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19
Q

What do bacteriostatic antibiotics do?

A

Inhibit bacteria so immune system can come and clear it

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20
Q

When are bacteriostatic antibiotics used?

A

○ Used when the host defense mechanisms are intact

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21
Q

What do bactericidal antibiotics do?

A

Kill bacteria

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22
Q

When are bactericidal antibiotics used?

A

○ Used when the host defense mechanisms are impaired

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23
Q

What are bactericidal antibiotics required in?

A

Required in endocarditis, kidney infection

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24
Q

What are the 2 spectrums of activity of antibiotics?

A
  1. Broad spectrum antibiotics

2. Narrow spectrum antibiotics

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25
What are broad spectrum antibiotics effective against?
○ Effective against many types of bacteria 
26
What are narrow spectrum antibiotics effective against?
○ Effective against very few types of bacteria
27
Refinement of cephalosporins over 3 generations
1. First generation cephalosporins  ○ Not good against gram-negative bacteria  ○ Good at killing gram-positive bacteria  2. Second generation cephalosporins  ○ Better at killing gram negative bacteria  ○ Lost ability to kill other microorganisms as effectively as before 3. Third generation cephalosporins  ○ Not good at killing gram positive bacteria   
28
What is the active structure of beta lactam antibiotics?
○ Contain beta-lactam rings which is the active structure in the drugs 
29
What do some beta lactam antibiotics act as?
○ Act as natural competitor substrates to the enzymes that make the bacterial cell wall
30
What do you divide antibiotics into how they work?
1. Cell wall synthesis inhibitors 2. Protein synthesis inhibitors 3. DNA/RNA processing inhibitors 4. Folic acid metabolism inhibitors 5. Cell membrane damaging drugs 6. Free radical generators
31
What are cell walls made of and what happens if it can make a cell wall?
○ Cell wall is made of peptidoglycan  | § If bacteria can't make cell wall, it wukk die
32
What do antibiotics that are protein synthesis inhibitors do?
Some antibiotics bind to 50s subunit whilst others bind to 30s subunit 
33
Why do antibiotics that bind to ribosomes have a good selective toxicity?
○ Antibiotics can bind to bacterial ribosomes without affecting eukaryotic ribosomes as they are different in structure
34
What do antibiotics that inhibit DNA/RNA processing inhibit?
○ Inhibits either the way in which the bacteria makes its DNA or mRNA
35
Why do antibiotics that are DNA/RNA processing inhibitors, show good selective toxicity?
○ Enzymes in bacteria are different to eukaryotic enzymes so these inhibitors show good selective toxicity 
36
What do quinolones inhibit?
Inhibits DNA gyrase which is a topoisomerase; helps DNA to coil and uncoil when DNA is replicating 
37
What is rifampin a key drug in treating?
§ Key drug in treating TB 
38
What is rifampin used prophylactically for?
§ Used prophylactically for meningitis as well 
39
What does rifampin target?
§ Targets enzyme that makes MRNA (DNA dependent DNA pol)
40
What happens if bacteria cannot make folic acid?
○ If bacteria cannot make this, it loses its cofactor for many processes so will die 
41
Why are cell membrane damaging drugs toxic to us?
○ Bacteria has similar cell membrane to eukaryotes so these drugs are toxic to us – poor selective toxicity 
42
What do free radicals damage?
Free radicals will damage multiple targets, not just one  | -Damages DNA and membranes
43
What do gram positive bacteria have massive structures of?
○ Massive structure of peptidoglycan  | § Consisting of cross linked peptides and polypeptides 
44
Why are antibiotics able to get inside the bacteria and what do they target?
○ Peptidoglycan structure is porous so plenty of antibiotics can get inside to do their job – target enzymes that put together the peptidoglycan structure 
45
What do the antibiotics that inhibit cell wall synthesis target?
Antibiotics that inhibit cell wall synthesis target enzymes that make the peptidoglycan layer
46
Where does the peptidoglycan layer in gram negative bacteria sit and with what?
sits in the periplasmic space with an outer membrane 
47
What mechanism do things that have to enter gram negative bacteria use?
§ Anything that has to go through it has to use transport mechanism 
48
Why can't many antibiotics be used on gram negative bacteria?
Many antibiotics cannot be used on gram negative bacteria because they cannot pass the barrier 
49
Peptidoglycan structure
• Made of penta-peptides that are crosslinked together and hold the matrix together  § Matrix has long polysaccharide chain
50
How does bacteria make the structure of peptidoglycan?
• Starts by adding precursor monomer of a disaccharide with 5 peptides  § Last two peptides in the monomer are alanines: D-ALA • Once the terminal D-Alas are made, it undergoes transport mechanism across cytoplasm membrane by linking it to a lipid transport molecule  • Once monomer is transported, there is attachment of the 5 crosslinking AAs ○ This structrure can then be polymerized in the cell wall by enzymes ○ Enzymes recognize D-ALA, D-ALA and cleave the terminal D-ALA and links it to the penta-peptide 
51
What does the vancomycin antibiotic recognise and do?
○ Vancomycin for example recognizes the D-ALA, D-ALA and binds to it  § Once bound, the enzyme cannot get to the structure and make the peptidoglycan  
52
What is PBP?
this is a cross-linking enzyme  
53
What does PBP bind?
Enzymes that competitively bind penicillins and cephalosporins 
54
What do penicillins and cephalosporins synthesise?
○ They synthesise the peptidoglycan 
55
Action beta lactam on penicillin and what does this prevent?
• beta lactams need to be able to cross the membrane and then bind to and inhibit the PBP  § This prevents the bacteria from cross-linking 
56
What is most bacterias autolytic response when it can't make peptidoglycan?
Most bacteria have an autolytic response; if it cannot make peptidoglycan, it lyses itself
57
What is sulfonamides and what enzyme does it inhibit?
Is a folic acid inhibitor and it inhibits dihydropteroate synthetase
58
What is the structure of sulfonamide almost identical to and what effect does it have?
○ Sulfonamide structure is almost identical to the PABA molecule which is necessary to make tetrahydrofolic acid  § If this is not made, the bacteria dies 
59
What does trimethoprim block?
Trimethoprim blocks dihydrofolate reductase 
60
Why does trimethoprim have a good selective toxicity?
Humans have this enzyme but it is completely different to the bacterial enzyme so even though it is present, it does not harm the host enzyme
61
When do we use antibiotics?
1. Treatment of bacterial infections | 2. Prophylaxis
62
Route of administration of antibiotics for community infections
• Community infections are often treated orally by GP
63
Route of administration of antibiotics for serious infections
○ hospitalisation  - systemic treatment   § e.g. i/v   rapid delivery, high [blood] ○ Often unable to take oral – vomiting, unconscious, poor gut absorption due to trauma ○ i/v  with perivascular collapse (e.g. septicaemia ) ○ i/m injection - meningitis case
64
Route of administration of antibiotics for topical infections
○ Conjunctivitis, superficial skin infections, burns, antiseptic creams, heavy metal ointments
65
What is MIC?
• Concentration at which the antibiotic will kill or inhibit the growth of organism 
66
What does MIC depend on?
• This will depend upon the age, weight, renal and liver function of the patient and the severity of infection

Medical microbiology (14 decks)

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