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Core Infection, Immunity and Haematology | ME2362 > L2 - Part 2 Treatment of Bacterial Infection > Flashcards

L2 - Part 2 Treatment of Bacterial Infection Flashcards

1
Q

What is peptidoglycan composed of?

A

N-Acetyl-β-D-Glucosamine (NAG)
N-Acetyl-β-D-Muramic acid (NAM)

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2
Q

What is the role of the peptide stem in peptidoglycan structure?

A

The peptide stem connects to form interpeptide bridges that strengthen the peptidoglycan layer

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3
Q

How do penicillins affect peptidoglycan structure?

A

Penicillins target the enzymes responsible for forming the interpeptide bridges, weakening the bacterial cell wall

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4
Q

What are β-lactam antibiotics, and how do they work?

A

β-lactam antibiotics (e.g., Penicillins, Cephalosporins, Carbapenems, Monobactams) inhibit penicillin-binding proteins (PBPs), preventing cell wall synthesis.
They are only effective on actively dividing bacteria.

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5
Q

What are the risks of β-lactam antibiotics?

A

Common: Rash or gut issues in 1/10 patients.
Rare: Anaphylactic shock (1 in 100,000 patients).
Avoid Cephalosporins if allergic to Penicillins (15% cross-reactivity).

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6
Q

Why is the brain a difficult target for drug distribution?

A

The blood-brain barrier (BBB) has tightly joined endothelial cells with gap junctions, preventing diffusion of many substances into the brain.

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7
Q

How does meningitis affect drug distribution to the brain?

A

Meningitis increases the permeability of the meninges, allowing drugs like penicillin to reach therapeutic levels in the brain.

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8
Q

What is the mechanism of action of vancomycin?

A

Vancomycin binds to the D-Ala-D-Ala terminus of murein monomer units, preventing peptidoglycan polymerization.

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9
Q

What is the mechanism of action and clinical use of vancomycin?

A

Binds to D-Ala-D-Ala terminus of murein monomer units, preventing peptidoglycan polymerization.
Used for treating Methicillin-resistant Staphylococcus aureus (MRSA).

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10
Q

What are the limitations of vancomycin?

A

Ineffective against Gram-negative bacteria due to inability to penetrate the outer membrane.

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11
Q

Does vancomycin show synergy with other antibiotics?

A

Yes, it shows synergy with aminoglycosides.

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12
Q

How do aminoglycosides inhibit protein synthesis

A

Bind to the 30S ribosomal subunit and cause misreading of mRNA, leading to incorrect protein synthesis.

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13
Q

What is the mechanism of macrolides and clindamycin?

A

Bind to the 50S ribosomal subunit and prevent translocation along mRNA, halting protein elongation

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14
Q

How do tetracyclines affect protein synthesis?

A

Interfere with the attachment of tRNA to the ribosome, blocking protein synthesis

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15
Q

What is the action of chloramphenicol on ribosomes?

A

Binds to the 50S ribosomal subunit and inhibits peptide bond formation, preventing protein elongation.

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16
Q

What is the mechanism of action of tetracyclines?

A

Interfere with the attachment of tRNA to the ribosome, preventing protein synthesis.

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17
Q

Where are tetracyclines produced?

A

Produced by Streptomyces bacteria, which are found in soil

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18
Q

What is the effect of tetracyclines on bacterial growth?

A

They are bacteriostatic, meaning they inhibit bacterial growth but do not kill the bacteria, which can interfere with the action of penicillins.

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19
Q

Why is tetracycline resistance widespread?

A

Due to extensive use and misuse, leading to bacterial resistance.

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20
Q

Why are tetracyclines contraindicated during pregnancy, breastfeeding, and in young children?

A

Tetracyclines bind to Ca²⁺ in bones and teeth, interfering with bone development and potentially causing permanent tooth discoloration.

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21
Q

How does food affect the absorption of tetracyclines?

A

Uptake is inhibited by certain foods, particularly those containing calcium, iron, or magnesium.

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22
Q

What is a potential side effect of tetracyclines due to their broad-spectrum nature?

A

They can lead to superinfections, such as Candida overgrowth, due to disruption of normal flora.

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23
Q

How do aminoglycosides affect protein synthesis?

A

Aminoglycosides, like streptomycin and gentamicin, change the shape of the 30S ribosomal subunit, causing misreading of mRNA and premature termination of protein synthesis.

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24
Q

What is the synergy between aminoglycosides and penicillins/vancomycin?

A

Penicillins/vancomycin destabilize the bacterial cell wall, increasing aminoglycoside access to the cell, enhancing their effectiveness.

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25
Q

How do aminoglycosides bind to the ribosome?

A

Aminoglycosides bind to the 30S ribosomal subunit, introducing a slight ‘bump’ that forces misreading of mRNA

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26
Q

What are the potential side effects of aminoglycosides?

A

Aminoglycosides can cause ototoxicity, leading to ear complications and hearing loss.

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27
Q

How do macrolides and clindamycin affect protein synthesis?

A

They bind to the 50S ribosomal subunit and prevent translocation along mRNA.

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28
Q

What are the uses of macrolides like erythromycin, clarithromycin, and azithromycin?

A

They target intracellular bacteria (e.g., Legionella, Chlamydia, Mycobacteria) due to their ability to penetrate membranes.
They are good alternatives for patients with a penicillin allergy, as they have a similar spectrum.

29
Q

How does chloramphenicol affect protein synthesis?

A

It binds to the 50S ribosomal subunit and inhibits peptide bond formation.

30
Q

What are the characteristics and uses of chloramphenicol?

A

It has a broad spectrum and is highly lipophilic, allowing good tissue penetration.

31
Q

What are the side effects of chloramphenicol?

A

It can inhibit liver enzyme p450 synthesis.
In neonates, underdeveloped hepatic function leads to high drug concentration, interfering with mitochondrial ribosomes, causing Grey Baby Syndrome (40% mortality).

32
Q

How does the lipophilic nature of chloramphenicol contribute to Grey Baby Syndrome?

A

Chloramphenicol’s lipophilicity allows it to cross plasma membranes and enter mitochondria, where it disrupts mitochondrial ribosomes, impairing aerobic respiration and leading to tissue hypoxia.

33
Q

How do different antibiotics target protein synthesis?

A

Aminoglycosides: Bind to the 30S ribosome, causing misreading of mRNA.
Macrolides and Clindamycin: Bind to the 50S ribosome and prevent translocation along mRNA.
Tetracycline: Interferes with the attachment of tRNA to the ribosome.
Chloramphenicol: Binds to the 50S ribosome and inhibits peptide bond formation.

34
Q

What do Fluoroquinolones inhibit?

A

Inhibit: Gyrase and topoisomerase.
Effect: Disrupts DNA supercoiling and replication.

35
Q

How do Fluoroquinolones work synergistically with β-lactams?

A

Synergy: Fluoroquinolones enter bacterial cells through pores.
Enhances effect: Works alongside β-lactams for better bacterial targeting.

36
Q

How do Fluoroquinolones affect intracellular bacteria?

A

Intracellular action: Accumulates in macrophages and neutrophils.
Effective against: Intracellular bacteria, e.g., Legionella.

37
Q

What are the side effects of Fluoroquinolones?

A

Cartilage erosion: Avoid in pregnancy and children under 18.
Liver enzyme inhibition: Can increase the availability of drugs like Warfarin.

38
Q

What is a side effect of Rifampicin?

A

Resistance: Develops rapidly; used in combination with other antimicrobials.

39
Q

How does Rifampicin affect contraceptive pills?

A

Induces p450 enzyme: Increased metabolism of the pill, reducing its efficacy.

40
Q

What is the mechanism of action of Rifampicin?

A

Blocks RNA polymerase: Prevents transcription and RNA synthesis.

41
Q

What is the bactericidal activity of Rifampicin?

A

Bactericidal: Effective against mycobacteria, Gram-positive (G+), and Gram-negative (G-) bacteria.

42
Q

How does Rifampicin act on intracellular bacteria?

A

Intracellular action: Accumulates inside cells and acts on intracellular bacteria, e.g., Tuberculosis and Leprosy.

43
Q

How does Rifampicin affect RNA synthesis?

A

RNA polymerase inhibition: Blocks RNA polymerase, preventing RNA from being made.

44
Q

What is the mechanism of action of Metronidazole?

A

Binds and disrupts DNA: Causes DNA damage in bacteria.

45
Q

Is Metronidazole bactericidal?

A

Bactericidal: Effective against both bacteria and amoebae

46
Q

What types of bacteria does Metronidazole act on?

A

Anaerobic bacteria: Specifically targets anaerobic bacteria.

47
Q

What is the Disulfiram effect of Metronidazole?

A

Disulfiram effect: When combined with alcohol, it causes nausea, vomiting, cramps, and vertigo.

48
Q

How does Metronidazole work at the molecular level?

A

Reactive nitric oxide group: Metronidazole has a highly reactive group that attacks DNA.

49
Q

What is the role of folate in bacteria?

A

Folate: Required for DNA synthesis and amino acid synthesis in bacteria.

50
Q

Where do we get folate, and how do bacteria obtain it?

A

Humans: Obtain folate from the diet.
Bacteria: Have a separate “Folate synthesis pathway.”

51
Q

What is the mechanism of action of Sulfonamides?

A

Sulfonamides: Structural analogues of PABA (a key substrate in folate synthesis) that bind and block DHPS (Dihydropteroate Synthase).

52
Q

What is the mechanism of action of Trimethoprim?

A

Trimethoprim: Inhibits DHFR (Dihydrofolate reductase) in the same folate synthesis pathway.

53
Q

How do Sulfonamides and Trimethoprim work together?

A

Synergy: Both target different steps in the folate synthesis pathway, resulting in a combined inhibition of DNA and amino acid synthesis.

54
Q

Why is folate important for bacteria?

A

Folate: Essential for DNA synthesis and amino acid synthesis in bacteria.

55
Q

How do humans obtain folate?

A

Humans: Obtain folate from the diet.

56
Q

What is the role of PABA in bacteria?

A

PABA (P-aminobenzoic acid): Used by bacteria in their folate synthesis pathway.

57
Q

What are Sulfonamides and how do they work?

A

Sulfonamides: Structural analogs of PABA, blocking the bacterial folate synthesis pathway.

58
Q

How do Trimethoprim and Sulfonamides work together?

A

Synergy: Sulfonamides block DHPS, and Trimethoprim inhibits DHFR, both acting in the folate synthesis pathway.

59
Q

When should Sulfonamides and Trimethoprim not be used?

A

Cannot be used with pus: Dead cells create an environment rich in amino acids and nucleotides, reducing efficacy.

60
Q

What is Kernicterus, and how is it related to Sulfonamides?

A

Kernicterus: Caused by Sulfonamides displacing bilirubin from albumin, leading to toxic bilirubin accumulation in the brain, especially in newborns.

61
Q

What type of antibiotic is Polymyxin (Colistin)?

A

Polymyxin: Cationic peptide antibiotic with both hydrophilic and lipophilic groups.

62
Q

How does Polymyxin target Gram-negative bacteria?

A

Polymyxin: Attracted to negatively charged lipopolysaccharides (LPS) on the outer membrane of Gram-negative bacteria.

63
Q

How does Polymyxin affect the bacterial membrane?

A

Action: Acts as a detergent, disrupting and permeabilizing the bacterial membrane.

64
Q

Why is Polymyxin not widely used?

A

Side effects: Serious neurotoxicity and ototoxicity.
Low volume of distribution: Not well absorbed from the GI tract.

65
Q

When is Polymyxin used therapeutically?

A

Topical use: For treating ear and skin infections.
Gut sterilization: Due to poor absorption, effective for sterilizing the gut.

66
Q

What makes Polymyxin effective against bacterial membranes?

A

Mechanism: The detergent-like structure disrupts membranes, forming aggregates that destabilize the membrane.

67
Q

What is the target of Isoniazid?

A

Target: Enzyme responsible for the assembly of mycolic acids in the outer membrane of mycobacteria.

68
Q

What is the distribution of Isoniazid?

A

Distribution: Penetrates host cells.

69
Q

What infection is Isoniazid used to treat?

A

Treatment: Primarily used for treating Tuberculosis.

Core Infection, Immunity and Haematology | ME2362 (7 decks)

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