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I&I WC1 > Antimicrobial resistance I > Flashcards

Antimicrobial resistance I Flashcards

This deck contains the lectures: Anti-microbial resistance in Gram- and Antimicrobial resistance in returning travellers,

1
Q

Mode-of-action

A
  • Cell wall synthesis
  • DNA, RNA & protein synthesis
  • Folic acid metabolism
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2
Q

Classes + representatives + mode-of-action

A
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3
Q

Why is the cell wall a good target for antibiotics?

A

Human cells don’t have a cell wall

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4
Q

What do all the B-lactams have in common structure-wise?

A

Ringstructure B-lactam

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5
Q

What are the members of the beta-lactam family?

A
  • Penicillins
  • Cephalosporins
  • Carbapenems
  • Monobactams
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6
Q

What can be said about the structure of the bacterial cell wall of gram-negative bacteria?

A

Gram-negative bacteria have a very thin layer of peptidoglycan + membrane in- AND out of their cell wall

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7
Q

On what structure do beta-lactams work?

A

Peptidoglycan

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8
Q
A
  • Sugar layer of NAM and NAG (sugar chains)
  • Connected via peptide bridges
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9
Q

The strength of the peptidoglycan network depends on …

A

It’s compactness, which itself depends on the length of the polysaccharide chains, the number of tetrapeptide bridges and on any hydrogen bonds that may form.

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10
Q

Key enzymes involved in the the peptidoglycan synthesis

A

Cytoplasm: smaller parts are made –>

Cell surface stage

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11
Q

What are the Penicillin Binding Proteins?

A
  • Transglycosylases
  • Transpeptidase
  • Carboxypeptidases
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12
Q

Where are the Penicillin Binding Proteins anchored?

A

In cytoplasmic membrane

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13
Q

Why do beta-lactams kill bacterial cells?

A

11 min

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14
Q

Explain the fragile dynamic balance between synthesis and hydrolysis of PG

A
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15
Q

Lytic enzymes or autolysins

A
  • Glycosidases
  • N-acetyl-muramyl-L-alanine amidases
  • Endopeptidases
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16
Q

On what does the bactericidal effect depend?

A

lytic enzymes, involved in
breaking down and rearranging PG

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17
Q

Beta-lactams work especially on active bacteria

A
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18
Q

Differences in activity among the various β-lactams depends on..

A

Penetration of the Gram-negative cell
Lability to periplasmic β-lactamases
Affinity to the PBPs

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19
Q

Mechanisms of resistance to β-lactam antibiotics (3)

A
  • Impaired permeability of outer membrane
  • Mutated PBPs with changed affinity
  • Enzymatic hydrolysis of the β-lactam ring
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20
Q

Penetration of β-lactams into Gram-negative bacteria

A
  • Passage via porins
  • Physicochemical factors influencing penetration
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21
Q

What is a porin and what is critical for the activity of B-lactams

A

-A porin is a transmembrane protein

Speed of diffusion of β-lactams through the porins is critical for their activity

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22
Q

Physicochemical factors influencing penetration (3)

A

-hydrophobicity
-the size of the molecule
-charge

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23
Q

Where can the B-lactamase come from?

A
  • Chromosome
  • Plasmid
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24
Q

What can the expression patterns of B-lactamases orginating from the chromosome?

A
  • Inducible
  • Constitutive
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25
Q

Example of inducible / phenotype

A

cephalosporinase

26
Q

Example of constitutive /phenotype for chromosome and plasmids

A

penicillinase

27
Q

What can the expression patterns of B-lactamases orginating from plasmids?

A

Constitutive

28
Q

If the enzyme is only effective against penicillin, you can use the other categories

A
29
Q

Extended spectrum beta-lactamases?

A

22min

30
Q

SHV-1

A
31
Q

Why are aminoglycosides suitable for use in humans?

A

Difference in ribosomal subunits between humans and bacteria

32
Q

Derivatives of micin and mycin

A
33
Q

Mechanism of aminoglycoside Action

A

Energy-independent phase
Energy-dependent phase
Binding to the 30S ribosomal subunit !! (most important for exam)

34
Q

Energy-independent phase

A

electrostatic binding to the outer membrane

35
Q

Energy-dependent phase

A

transport into the cytoplasm by PMF (transmembrane electrical potential)

36
Q

Binding to the 30S ribosomal subunit !! (most important for exam)

A

inhibition of protein synthesis
misreading of the codons

37
Q

What does PMF mean?

A
38
Q

Mechanisms of resistance to aminoglycosides

A

Aminoglycoside-modifying enzymes (most important!!)
Alteration in uptake
Change in ribosomal binding sites (methyltransferases)

39
Q

Name the three categories of aminoglycoside-modifying enzymes

A

AAC: acetyltransferases
ANT: adenyltransferases
APH: phosphotransferase

40
Q

AAC: acetyltransferases

A

acetyl CoA-dependent acetylation of an amino group

41
Q

ANT: adenyltransferases

A

ATP-dependent adenylation of an hydroxyl group

42
Q

APH: phosphotransferase

A

ATP-dependent phosphorylation of an hydroxyl group

43
Q

DNA: guinolones, why very powerful and widely used?

A

Many of these can be taken as tablets and are still sufficiently absorbed and bactericidal –> perfect penetration of tissue

44
Q

Uptake of quinolones into the bacterium

A
45
Q

Mechanism of action of quinolones

A
46
Q

Role of topoisomerases

A
  • Regulate the super-coiling of DNA.
  • Cuts dsDNA to initiate replication.
47
Q

Mechanisms of resistance
(chromosomally-encoded) quinolones

A
  • Decreased target-affinity
  • Decreased accumulation
48
Q

Decreased target-affinity

A

Mutations in DNA-gyrase and topoisomerase IV
- Mutations in ‘quinolone resistance-determinating region (QRDR)’

49
Q

Decreased accumulation

A
  • Decreased porine-expression (low-level resistance)
  • Hyper-expression of natural efflux
50
Q

Mechanisms of resistance (Plasmid-mediated resistance) quinolones

A
  • qnrA
  • Aminoglycoside acetyltransferase
  • Quinolone efflux pumps
51
Q

How does qnrA work?

A

Binds to DNA gyrase and topoisomerase IV, leading to inability for quinolones to bind

52
Q

Patient being hospitalized abroad have a higher chance of bringing MDROs

A
53
Q

Prevalence of MDROs

A

Africa
West-Pacific
Southern Asia

54
Q

Study protocol

A

Healthytravelers included via travel clinics
2001 travelers
215 household members

Sample kit directly before and after travel
Fecal swabs

Follow up for 12 months
1, 3, 6 and 12 months after return

55
Q

Risk factors MDRO acquisition

A

Antibiotic use during travel
Traveller’s diarrhoea
Meal at street food stalls

56
Q

Protective factors MDRO acquisition

A

Daily hand washing before meals
Beach holidays

57
Q

Leading risk factors for acquisition of MDR-E are

A

Travel to SouthernAsia
Antibiotic use during travel
Traveller’s diarrhoea

58
Q

Hospitals: unknown carriage could lead to? (3)

A
  • Difficulty treating infections
  • Hospitalization without the appropriate infection prevention and control measures
  • Spread to other patients, healthcare personnel and the hospital environment
59
Q

Which division can be made in-hospital (nosocomial) transmission?

A
  • Direct transmission
  • Indirect transmission
60
Q

How is direct transmission established in the hospital?

A

Patient-to-patient, patient-to-healthcare personnel

61
Q

How is indirect transmission established in the hospital?

A

Hospital environment, medical devices

62
Q

What is the current MDRO screening strategy?

A

Universal risk assessment with risk-based screening

I&I WC1 (25 decks)

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