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Antibiotics Flashcards

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1
Q

What are antibiotics?

A

Natural products of fungi and bacteria - soil dwellers

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2
Q

What is the effect of antibiotics on bacteria?

A
  • natural antagonism and selective advantage

- kill or inhibit growth of other microorganisms

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3
Q

How are antibiotics produced?

A

Most derived from natural products by fermentation, then modified chemically

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4
Q

Why are antibiotics chemically modified?

A

↑ pharmacological properties

↑ antimicrobial effect

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5
Q

Name an example of totally synthetic antibiotics

A

Totally synthetic - e.g. sulphonamides

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6
Q

What allows the selective toxicity in antibiotics?

A
  • Differences in structure and metabolic pathways between host + pathogen
  • Harm microorganisms, not host
  • Target in microbe, not host (if possible)
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7
Q

When s selective toxicity an issue for antibiotics?

A
  • Difficult for viruses (intracellular), fungi + parasites

- Variation between microbes

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8
Q

Describe the therapeutic margin of antibiotics

A 
Active dose (MIC)  Vs. Toxic effect
Narrow for toxic drugs e.g. aminoglycosides, vancomycin ototoxic, nephrotoxic
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9
Q

What is the effect of antibiotics on microbial antagonism?

A

Maintains flora - complex interactions
Competition between flora

Limits growth of competitors and PATHOGENS

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10
Q

Describe the consequences of antibiotics on microbial antagonism

A

Some antibiotics disrupt ecosystem; Loss of flora → bacterial or pathogen overgrowth
e.g. Antibiotic Associated Colitis

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11
Q

Which antibiotics can cause antibiotic associated collitis?

A

Clindamycin
Broad-spectrum lactams
Fluoroquinolones
> Cause pseudomembranous colitis

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12
Q

How much of the normal gut flora does C.difficile compose?

A

Clostridium difficile (part of normal flora of 3% of population)

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13
Q

What is pseudomembranous colitis?

A

Pseudomembranous colitis: Clostridium difficile overgrowth

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14
Q

What are the symptoms of pseudomembranous colitis?

A

Ulcerations – inflammation
Severe diarrhoea due to inability to absorb water
Serious hospital cross-infection risks

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15
Q

How is bacterial clearance achieved?

A

Antibiotic + immunity → bacterial clearance

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16
Q

Who classifies as an immunosuppressed patient?

A
  • Cancer chemotherapy
  • Transplantations
  • Myeloma, leukaemias
  • HIV w/ low CD4
  • Neutropenics
  • Asplenics
  • Renal disease
  • Diabetes
  • Alcoholics,
  • Babies, elderly
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17
Q

How are antibiotics classified?

A
  • Type of activity
  • Structure
  • Target site for activity
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18
Q

What are bactericidal antibiotics?

A

Kill bacteria
Used when host defense mechanisms are impaired

Required in endocarditis, kidney infection

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19
Q

What are bacteriostatic antibiotics?

A

Inhibit bacteria
Used when host defense mechanisms are intact

Used in many infectious diseases

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20
Q

What are broad spectrum antibiotics?

A

Effective against many types

Example: Cefotaxime

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21
Q

What are narrow spectrum antibiotics?

A

Effective against very few types

Example: Penicillin G

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22
Q

How can the same antibiotic family be used to treat different types of bacteria?

A

3 different drugs; cephalosporins (penicillin)

Chemically modified to give different biological properties (1/2/3rd gen) to treat

  • Gram -ve E.coli
  • Gram +ve Streptococci (pneumoniae)
  • Gram +ve staphylococcus
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23
Q

Why do we use different antibiotics for Gram +/-ve bacteria?

A

Have different structures so require different mechanisms of action to overcome

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24
Q

How are antibiotic families classed?

A

Antibiotics are classified in families based on their structures

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25
What is the significance of antibiotic families?
Important to know for: - Drug resistance - Classification
26
How do families of antibiotics work?
Structural mimics of natural substrates for enzymes e.g. - β-lactams Penicillins and cephalosporins contain β-lactam rings ∴ are informally called β-lactams
27
How do bacteria become resistant to β-lactams ?
Some bacteria develop β-lactamase enzymes that degrade the β-lactam structure making these antibiotics non-functional in treatment
28
How does bacterial structure effect antibiotic selective toxicity?
There are many targets for selective toxicity Bacteria have complex multimeric structures with complex metabolisms Structures only in bacteria are good antibiotic targets
29
What are the bacteria targets for common antibiotics?
- Cell wall synthesis - Free radicals - DNA/RNA processing - Protein synthesis - Cell membrane - Folic acid synthesis
30
Give examples of cell wall synthesis antibiotics
Cell wall synthesis antibiotics e.g: (β-lactams) and Vancomycin (kept in reserve to treat MRSA) Very potent
31
Name examples of protein synthesis inhbiitors
Erythromycin, chloramphenicol (eye drops, topical drug v. toxic not given IV)
32
Explain the selective toxicity of protein synthesis inhibitors
Bind to different ribosomal subunits; can inhibit bacterial ribosomes without inhibiting eukaryotic ribosomes - safe; good selective toxicity
33
How do DNA / RNA processing antibiotics work?
Inhibit DNA replication / RNA production - these mechanisms differ ∴ provides selective toxicity to enzymes involved
34
What is DNA gyrase?
DNA gyrase is a topoisomerase (different to eukaryotes) responsible for (un)coiling during DNA replication
35
Give examples of DNA/RNA processing antibiotics and their roles
Rifampin - key drug against TB, targets DNA-directed RNA Pol producing mRNA Quinolones (e.g. ciprofloxacin etc.) v. potent DNA Gyrase inhibitors
36
Describe the selective toxicity of folic acid synthesis antibiotics
Bacteria synthesise their own folic acids | V. good selective target as humans don’t contain folic acid producing enzymes
37
How do folic acid synthesis antibiotics work?
Antibiotics inhibit folic acid production causing bacteria to lack of co-factors for vital chemical reactions
38
Give an example of a useful cell membrane antibiotic
E.coli gram -ve bac. that cause UTIs are resistant to almost every antibiotic except for colistin However colistin is v. toxic; only used when necessary
39
Describe the selectivity of free radical antibiotics
Antibiotics that generate free radicals have multiple targets throughout bacterial cell e.g. metronidazole (fights anaerobes)
40
What is peptidoglycan?
A crosslinking structure of peptides and polysaccharides
41
Describe the outer structure of a Gram +ve bacteria
Massive peptidoglycan structure on top of bacteria membrane Multiple other cell wall components e.g. teichoic and lipoteichoic acids - equivalent of exotoxin LPS
42
How do cell wall synthesis antibiotics work?
Antibiotics (β-lactams) that inhibit cell wall synthesis, target enzymes that form peptidoglycan
43
Describe the Gram-ve bacteria outer layers
Gram -ve also have peptidoglycan but it resides in the periplasmic space with an outer membrane - impermeability barrier; only way nutrients, ions etc. get through is via porins
44
Why are some antibiotics useless on gram -ve bacteria?
Many antibiotics can’t be used on gram -ve bacteria as they can’t infiltrate the impermeable outer membrane barrier
45
How is peptidoglycan formed?
This structure is put together by a series of enzyme reactions
46
Why does each bacteria have a different peptidoglycan structure?
Different bacteria have varying peptidoglycan structures ∴ the enzymes forming them have slightly different specificities
47
Describe the structure of a general peptidoglycan
Composed of (penta) polypeptides that are crosslinked to hold a matrix with long polysaccharide (n acetylglucosamine) chains together
48
Outline the process of peptidoglycan formation
1. Peptidoglycan precursor: disaccharide w/ 5 peptides and terminal D-ala-D-ala isomers (D-alanines) 2. Precursor transported across cytoplasmic membrane by linking to lipid transport molecule 3. Precursor joins pentameric a.a. structure 4. Cell wall transcarboxypeptidases polymerise by recognising + cleaving terminal D-ala’s 5. Terminal D-ala linked to end of pentapeptide 6. Pentapeptide linked to next monomer’s D-ala which also has terminal D-ala cleaved
49
What is the significance of the peptidoglycan D-ala-D-ala terminus?
D-ala-D-ala required for crosslinking to occur and are specific to peptidoglycan synthesis in bacteria
50
How do some antibiotics inhibit peptidoglycan formation?
Certain antibiotics (cycloserine) block terminal D-ala’s production Others prevent precursor transport
51
What enzyme provides β-lactams selective toxicity against peptidoglycan formation?
Trans-carboxypeptidases are good antibiotic targets of β-lactams as not present in human cells - specific to bacteria
52
How does vancomycin inhibit cell wall synthesis?
Vancomycin recognises D-ala-D-ala and binds to it, preventing peptidoglycan formation
53
What is a PBP?
Penicillin binding proteins (crosslinking enzymes) synthesise peptidoglycans and competitively bind to cephalosporins + penicillins etc.
54
How do β-lactams cause their effect?
When β-lactams administered, they have to cross the porin and bind + inhibit the PBP
55
What is the effect of a successful β-lactam?
If able to target PBP, the antibiotic can prevent bacteria from crosslinking, causing an autolytic response
56
Outline features of the folic acid synthesis inhibitors
Combinations are synergistic and bactericidal - Gram +ve and G-ve - Nocardia + toxoplasma - UTI - Broad spectrum
57
How do sulfonamides inhibit folic acid synthesis in bacteria?
Sulfonamides (antibiotics- competitive inhibitor) inhibit dihydropteroate synthetase enzyme that is specific to bacteria Structure almost identical to PABA (recursor) of tetrahydrofolic acid
58
Outline how folic acid synthesis inhibitors provide selective toxicity
Humans ingest in diet Dihydrofolic acid (Vit.b9) Humans have dihydrofolate reductase enzyme ; converts dihydrofolic acid (vit.b9) → tetrahydrofolic acid -completely different to bacterial enzyme ∴ trimethoprim (antibiotic) has little effect against host enzyme but high affinity against bacterial enzyme
59
Describe the use of antibiotics
- Treatment of bacterial infections - Prophylaxis - Inappropriate use; viral sore throats; patient pressure
60
Outline how antibiotics are used for prophylaxis
- close contacts of transmissible infections - Decreased carriage rates (↑ ~80% in outbreaks) e.g. meningitis - prevention of infection e.g. tuberculosis - peri-operative cover for gut surgery - people with ↑ susceptibility to infection
61
How are community infections treated?
Community infections often treated orally by GP
62
How are serious infections treated?
Hospitalisation - systemic treatment e.g. i/v rapid delivery, high [blood] often unable to take oral – vomiting, unconscious, poor gut absorption due to trauma
63
How are topical infections treated?
conjunctivitis, superficial skin infections, burns, antiseptic creams, heavy metal ointments
64
What does antibacterial MIC dose depend upon?
- Age, weight, renal + LFT of patient and infection severity - Susceptibility organism - Antibiotic properties i.e. MIC

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