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IPM > Antibiotic Classes & Modes of action > Flashcards

Antibiotic Classes & Modes of action Flashcards

1
Q

Macrolides and examples. State Mechanism, What it’s active against. Bacteriostatic or sidal?

A

Bind to 50s subunit of ribosomes; inhibiting peptidyl transferase and so blocking peptide elongation.

Macrolides are generally good for respiratory infections and soft tissues as it can penetrate human tissues well. It’s an alternative to penicillin allergic patients.

e.g Erythromycin and Clarithromycin

Erythromycin: in particular and is also used for staphylococcal infections

Clarithromycin, a derivative of erythromycin, is used along the same lines but has additional activity e.g. against Legionellaspecies and chlamydiae.

Bacteriostatic. Can be Bactericidal at high concentrations.

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2
Q

Chloramphenicol - Activity - Side effects - susceptible microorganisms. Static or Sidal?

A

Diffuses across cell membrane and Binds to 50s subunit of ribosomes inhibits protein synthesis inhibits peptidyl transferase, so no peptide elongation. In terms of activity - it has broad-spectrum range activity.

Penetrates the cerebrospinal fluid well, Therefore it’s used to treat meningitis.

It is Bacteriostatic, but when treating gram +ve cocci, it is bactericidal

Side effect: a bone marrow does not produce cells

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3
Q

Tetracyclines. action - indication - examples and side effects. Static or Sidal?

A

Bind to 16s subunit of ribosomes but interefers with 30s ribosome subunit, inhibiting tRNA.

e.g doxycycline

Indicated for Acne Vulgaris,

Side Effects: Nausea, Diarrhoea and Renal Concern. It can accumulate in bones and teeth. Teratogenic.

Bacteriostatic

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4
Q

Oxazolidinones

A

Bind to 50s subunit of ribosomes; inhibit tRNA binding

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5
Q

Rifamycins MOA/Activity/Side effects

A

inhibit bacterial DNA-dependent RNA polymerase, preventing transcription of mRNA

Activity: Rifampicin crosses the BBB and is used to treat meningitis

It’s Broad Spectrum and can be used on both G+ve and G-ve Can also be used in combo with isoniazid for Mycobacterium Tuberculosos

Side Effects: Fever, Loss of Appetite, Malaise

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6
Q

Quinolones

A

Inhibit topoisomerases

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7
Q

Nitroimidazoles

A

Reduction in anaerobes produces radicals which cause oxidative damage to macromolecules e.g Metronidazole

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8
Q

isoniazid

A

inhibits mycolic acid synthesis in Mycobacteria

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9
Q

Bacitracin

A

inhibits regeneration of lipid barrier

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10
Q

cycloserine

A

inhibits D-Ala-D-Ala formation

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11
Q

Glycopeptides and an example. What are they only effective against? Indications?

A

prevention of incorporating subunits into growing peptidoglycan wall by binding to the D-ala D-ala of the short peptide chain on N-acetylmuramic acid

E.g Vancomycin

ONLY effective against Gram-positive (both anaerobes and aerobes) because they’re too bulky to penetrate outer membrane of the G-ve species

They’re reserved for seriously ill patients with G+ve species. e.g MRSA and C.difficule

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12
Q

name 3 B-Lactams

A

Penicillin, Cephalosporin, Carbapenems

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13
Q

Role of B-Lactams with an example

A

inhibit transpeptidase crosslinking of Peptidoglycan strands. Beta Lactam binds to penicillin-binding proteins.

This increases osmotic pressure, activating autolysins that degrade the cell wall.

There is a change in cell shape and size

Leads to the death of the bacterial cell

e.g Benzylpenicillin

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14
Q

Polymixims

A

disrupt bacterial membranes

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15
Q

Sulfonamides

A

DHTS (dihydropteroate synthetase) inhibitors

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16
Q

Trimethoprim

A

DHFR (Dihydrofolate reductase) inhibitor

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17
Q

Daptomycin

A

Disrupts Gram +ve plasma membrane

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18
Q

Bind to 50s subunit of ribosomes; blocking peptide elongation

A

Macrolides

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19
Q

Binds to 50s subunit of ribosomes; inhibits peptidyl transferase

A

Chloramphenicol

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20
Q

Bind to 30s subunit of ribosomes, inhibiting tRNA binding

A

Tetracyclines

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21
Q

Bind to 50s subunit of ribosomes; inhibit tRNA binding

A

Oxazolidinones

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22
Q

inhibit bacterial RNA polymerase

A

Rifamycins

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23
Q

inhibit topo-isomerases

A

Quinolones

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24
Q

Reduction in anaerobes produces radicals which cause oxidative damage to macromolecules

A

Nitroimidazoles

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25
Q

inhibits mycolic acid and synthesis in Mycobacteria

A

isoniazid

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26
Q

inhibits regeneration of lipid barrier

A

Bacitracin

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27
Q

inhibits D-Ala-D-Ala formation

A

cycloserine

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28
Q

prevention of incorporating subunits into peptidoglycan wall

A

Glycopeptides

29
Q

Penicillin, Cephalosporin, Carbapenems

A

name 3 B-Lactams

30
Q

inhibit transpeptidase crosslinking of Peptidoglycan strands

A

Role of B-Lactams

31
Q

disrupt bacterial membranes

A

Polymixims

32
Q

DHTS (dihydropteroate synthetase) inhibitors

A

Sulfonamides

33
Q

DHFR (Dihydrofolate reductase) inhibitor

A

Trimethoprim

34
Q

Disrupts Gram +ve plasma membrane

A

Daptomycin

35
Q

state all the classes of antimicrobial agents

A

Aldehydes

Oxygen species

Halogens

Phenoliccompounds

Alcohols

Biguanide-based compounds

Quaternary ammonium-based compounds

Organic acids

36
Q

what class is the most aggressive out of the Antimicrobial agents? give an example and how it works

A

Aldehydes, e.g Glutaraldehyde: It treats surfaces and temperature sensitive medical and dental equipment.

Works by cross linking proteins, This therefore prevents protein synthesis of microbial macromolecules. It shows broad efficacy of action, and is rapidly antibacterial, fungicidal, virucidal.

It is so active that it can be used as a chemosterilant.

Pros: Effective at low temperature, highly active and low surface corrosiveness

Cons: Can cause skin irritation

37
Q

name some broad spectrum antibiotics

A

(the three) B-Lactams, Tetracycline, Chloramphenicol, Quinolones, Macrolides

38
Q

name some narrow spectrum antibiotics

A

Glycopeptides, Aminoglycosides

39
Q

discuss an example of a biguanide based compound. comment on acivity, strengths and weaknesses

A

chlorhexidine. Antiseptic mouthwash used to treat a wound. It is rapidly absorbed through bacterial/yeast cells
- acts primarily on cell membranes = leads to cytoplasm content leakage

Thus - there is a loss of function and cell structure.

Chlorhexidine directly inserts into cell membrane bilayers

Activity: Broad spectrum antibacterial activity. Less effective against fungi.

Strengths: relatively little irritation of skin or mucous membranes. Effective in preventing spread of pathogens in hospitals.

Weaknesses: can cause eye problems and can damage the inner ear. It can also cause anaphylactic shock in extreme cases.

40
Q

what strategies emerged to deal with penicillinase producing strands? add examples

A
  1. design of penicillinase-tolerant penicillins e.g flucloxacillin
  2. development of penicillinase inhibitors e.g clavulanic acid, sulbactam and tazobactam

the penicillinase inhibitors have little antibacterial activity alone, but bind and inactivate beta-lactamases/penicillinases. Allows a combined approach of penicillin (antibiotic) + tazobactam (inhibitor)

41
Q

can penicillins target only G-ve/G+ve or Both?

A

both

42
Q

give the structure for clavulanic acid

A
43
Q

what is co-amoxiclav?

A

Amoxicillin - similar and often combined with clavulanic acid. It is active against certain gram negatives e.g H.influenzae. The addition of the B-lactamase inhibitor clauvulanic acid increases the spectrum of antimicrobial activity

44
Q

state the three locations on a bacterial ribosome for attack

A

APE:

A (aminoacyl) site - where after initiation each ‘new’ aminoacyl- tRNA attaches

P (Peptidyl) site - where the the peptide bonds are formed

E (Exit) site - where tRNA leaves the ribosome

45
Q

Aminoglycosides - Mode of action - Suseptible organisms - Side effects - drug examples

A

Aminoglycosides are actively transported into bacterial cells growing aerobically. They bind irreversibly to 30S subunit, Inhibiting protein synthesis. Interruption of translation results in misreading of mRNA. This leads to NO proteins or DEFECTIVE proteins.

They are active against staphylococci and mycobacteria. However they’re innefective against anaerobically respiring bacteria which have innate resistance.

indicated for Pseudomonas Aeruginosa

Examples are gentamicin, and streptomycin. Side effects: Renal Toxicity, Dizziness, Hearing loss, Nausea and Vomiting.

46
Q

What is a side effect of penicillins?

suggest a drug class (and examples in that) to give to a patient with a penicillin allergy.

A

S/E

rash, diarrhoea, abdominal pain, nausea, vomiting, hypersensitivity.

Alternatives

Macrolides - erythromycin and clarithromycin

47
Q

Antibiotics inhibiting nucleic acid synthesis have three main interrupting strategies. What are they?

A
  1. Binding to DNA Topoisomerases
  2. Preventing transcription by binding DNA-dependent RNA polymerase
  3. Distupting bacterial DNA through cytotoxicity
48
Q

what are the four overall strategies of bacteria activity. Give examples

A
  1. Disrupt bacterial cell walls - e.g Beta Lactams, Glycopeptides
  2. Inhibit protein synthesis e.g Aminoglycosides, Tetracyclines, Chloramphenicol, Macrolides, Clindamycin
  3. Inhibit nucleic acid synthesis e.g Quinolones, Rifampicin, Methonidazole
  4. antimetabolite activity e.g Trimethoprim, Sulfenamide
49
Q

Metronidazole indication - mode of action. Static or Sidal?

A

Indicated for C.Difficile and B. Fragilis. It is only active in anaerobic bacteria and the drug is cytotoxic. It converts oxidoreductase into a mutagenic product which binds to DNA and destbilises the DNA Helix, causing it to break.

Bactericidal.

50
Q

Give an overview of the mechanisms of antibiotic resistance

A
  1. Metabolic bypass-resistance (alters the enzyme in a metabolic pathway targeted by the abx)
  2. Over production ( the bacteria produces more of what is being targeted, so the abx is overwhelmed)
  3. Reduced uptake (e.g Beta-lactams reduced uptake)
  4. Efflux pumps (e.g S.Aureus has efflux pumps for fluoroquinolones)
  5. Alteration (e.g of the receptor or target site)
  6. Destroy the Abx (Beta-lactamases)
  7. Modify the Abx - e.g aminoglycosides made less able to produce oxidative radicals)
51
Q

name two elements of a bacteria that can be transferred by horizontal gene transfer

A

Plasmid

Transposons

52
Q

what are the pros and cons of multiple horizontal gene transfer?

A

There is an increased metabolic cost to the cell, this can affect cell fitness. However there is an increased ability for the cell to resist more than one of a particular number of antibiotic challenges

53
Q

State 4 ways we can maintain the effectiveness of antibiotics

A
  1. Make them less generally available (e.g prevent agricultural use)
  2. Antibiotic rotation
  3. Resistance surveillance
  4. stop innapropriate use of antibiotics
54
Q

name two Quinolones, Mode of action, activity, side effects

A

e.g Ciprofloxicin - Broad Spectrum

Fluoroquinolones - Narrow Spectrum (Gram Negative Enterobacteria, UTI)

In Gram -ve cells = DNA Gyrase is the target

In Gram +ve cells = Binds to DNA Toposiomerases to trap them. This affects supercoiling processes: Bacteriostatic.

if it breaks bacterial DNA this can result in cell death. Bactericidal

nausea, vomiting, diarrhoea, abdominal pain, headache, lethargy, insomnia

55
Q

What is Amphtotericin B and what’s it indicated for. State MOA

A

Broad Spectrum Antifungal. It exhibits selective toxicity Binding to the ergosterol in fungal cell wall membranes, not cholesterol in human cell walls. It damages the fungal membrane, causing pores. This compromises the membrane integrity, leading to leakage of fungal metabolites

Indicated for Candida Albicans

56
Q

Give an example of an azole drug, stating how they work

A

Terbinafine - Inhibits egosterol synthesis

57
Q

how does the malaria parasite operate and how are qunine and chloroquine throught to work?

A

As part of their cell cycle, malaria infects blood cells. They’ll use haemoglobin as a source of amino acids. Haem remains intact. The haem is toxic and they’ll detoxify it.

Both quinine and chloroquine are thought to act to prevent detoxification of haeme in the parasite > this means the haeme remains and as such is toxic ultimately through cell lysis.

58
Q

Clindamycin mode of action and what is it active against?

A

Binds to 50s subunit and inhibits protein elongation. Active against Staphylococcus (a G+ve) and Anaerobic G-ve

59
Q

How does Metabolic bypass give bacteria resistance? - Give an example

A

How?

Bacteria alters enzyme in the metabolic pathway targeted by the abx

Example?

Mutagens give bacteria -> trimethoprim-resistant variants of dihydrofolate reductase genes

∴ bacteria bypasses the block trimethoprim causes on the non-mutated version

60
Q

How does Overporduction give bacteria resistance? What example

A

How?

Bacterial cell makes more of what an abx is targeting:

Hence abx gets used up faster

Example?

Overproduction of a specific penicillin-binding protein (PBP-4)

e.g increases beta-lactam resistance in S. auereus by “mopping up’ the bacteria

61
Q

How does reduced uptake give bacteria resistance?

A

Bacterial cell takes LESS Abx

  • abx causes LESS damage to the bacteria
62
Q

How des efflux pumps give bacteria resistance? E.g?

A

How?

Efflux pumps to get rid of as much drug entering the bacterial cytoplasm as possible

Example

P.aeruginosa has multi-drug efflux pumps to efflux out many different types of abx

(Pseudomodas infections are hard to treat!)

63
Q

How does Alteration give bacteria resistance

A

How?

Bacteria alters the target site of abx

Example?

Mutations in chromosomal genes coding for ribosomal subunits can alter the abx target

64
Q

Give an example of how modifying the antibiotic give bacteria resistance

A

Aminoglycoside abx resistance is due to modification of Abx structure as a result of 3 classes of enzymes

65
Q

How do patients make antibiotic resistance worse?

A
  • Patient non-compliance can lead to -> resistance
    • By not completing their course -> suboptimal therapy, it makes bacteria sensitive to the Abx ∴ allows bacteria to emerge as resistant.
66
Q

Where on the bacterial genome has resistance arisen? How does this fit in the bacterial survival.

A

Firstly, Antibiotics are needed to give selective pressure and favour resistant strains in survivng.

  • Chromosome -> contains all genes required for cellular maintenance + growth
    • Only the specific bacteria will become resistant
  • Plasmid -> DNA molecule that replicates independently from the chromosome
    • Can move between cells -> CONJUGATION
      • of the same or DIFFERENT species!! > leads to acquired resistance
    • can be multi-drug resistant = THREATHENING! Thrives in hospitals where lots of Abx is used
67
Q

How do I maintain the effectiveness of currently available agents? What factor do we consider when choosing an antibiotic to use?

A

Maintain effectiveness

  1. Make Abx generally less available
  2. Abx rotations
  3. Resistance surveillance
  4. Stop inappropriate use of Abx use

Choosing an Antibiotic is based on

  1. Pathogen susceptibility
  2. Cost
  3. Side effects
  4. Impact on host microbiota
68
Q
A
69
Q

Give a whistle stop tour on how to select an Antibiotic for an infection

A

Selecting an Abx to Treat an Infection

First = Identify the pathogen -> via undertaking tests in the Diagnostic Microbiology Lab

  • Sample is received
  • The specimen is look under the microscope to see what pathogens are likely in the sample
  • This indicates what:
    • Growth condition should be used
    • Growth media should be used
  • After incubation -> colonies of pathogen are recognised by their phenotype, identifying the pathogen
  • Microscopy confirms OR denies this identify based on cell shapes + staining
    • Staining -> Gram +ve OR Gram –ve
    • Shapes -> Bacillus(rods) or Coccus (spherical)
  • Often a mixed culture. Next step = derive a pure culture

IPM (15 decks)

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