Session 5 - Antibiotics Flashcards

1
Q

How do antibiotics damage bacteria but not host cells?

A

By exploiting the differences that exist between the structure and physiology of the prokaryotic bacterial cells and the host eurkaryotic cells

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2
Q

What are two different overall mechanisms by which antibiotics effect bacteria

A

Bacteriostatic (inhibit bacterial growth)

Bacteriacidal (kill bacteria)

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3
Q

Give four sites on bacteria targeted by antibiotics

A

Peptidoglycan cell wall
Nucleic acids
Protein synthesis
Cytoplasmic membrane

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4
Q

Why can bacterial cell walls be targeted, and by which three main classes of AB?

A

Peptidoglycan cell wall only present in prokaryotic cell.

Penicillins
Cephalosporins
Glycopeptides

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5
Q

Why can nucleic acids be targeted, and by which three classes of AB?

A

Bacterial genome is a single, circular strand of DNA unenclosed by a nuclear envelope, in contrast to eukaryotic chromosomal arrangement within the nucleus Antifolates
Quinolones
Rifampicin

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6
Q

How can protein synthesis be targeted, and name three ABs which do thus

A
Bacterial ribosome (50s+30s subunits) is different to the mammalian ribosome (60s+40s subunits)	Aminoglycosides
Tetraclyclines
Macrolides
Chloramphenicol
Fusidic acid
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7
Q

How can the cell membrane of bacteria be targeted, and give 1 AB that does thus

A

Bacterial plasma membrane does not contain any sterols, unlike mammalian. Polymyxins

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8
Q

Give four primary reasons for prophylaxis of bacterial infections

A
o	Peri-operative (Prevention of surgical site infections)
o	Short term
	Meningitis contacts
o	Long term
	Asplenia (encapsulated bacteria)
	Immunodeficiency
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9
Q

Give two ways ABs can be used to treat significant bacterial iunfections

A

o Treatment of cultured, proven infection

o Empirical treatment of suspected infection

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10
Q

What is the ideal antibiotic? (2)

A

o Clean killing of infecting bacteria
 Minimal impact on non-target commensal organisms
 No resistance in any surviving pathogens
o No adverse effects on patient

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11
Q

Give 8 factors which help determine the likely infectious agent in an infection

A
o	Anatomical Site
o	Duration of illness
o	Past medical history
o	Occupational history 
o	Travel history
o	Time of year
o	Age
o	Personal background
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12
Q

Give four factors which determine which antibiotics are likely to be effective

A
o	Community or healthcare onset?
o	Severity of infection
o	Baseline rate of resistance
o	Immune status of patient
	Immunocompromised patients will need IV Antibiotics immediately
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13
Q

What three factors do you need to consider when choosing best antibiotic?

A

o Efficacy
o Cost
o Administration Route

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14
Q

Give some common antibiotic adverse drug reactions

A

Pharmcological (toxicities, drug interactions)
Allergic reactions
Impact on normal flora (c.diff)

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15
Q

What is therapeutic drug monitoring?

A

Therapeutic drug monitoring is used to ensure and adequate, non-toxic dose.

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16
Q

Give two antibiotics which require therapeutic monitoring

A

Gentomicin

Vancomycin

17
Q

What class of AB is gentomicin>

A

Aminoglycoside

18
Q

What are the effects of gentomicin?

A

 Dose related ototoxicity and nephrotoxicity at high plasma levels

19
Q

What type of AB is vancomycin?

A

Glycopeptide

20
Q

Give five side effects of vancomycin

A

 Dose related ototoxicity and nephrotoxicity at high plasma levels
 Fever, rashes
 Local phlebitis at site of infection

21
Q

Give two overarching methods via which bacteria develop AB resistance

A

Chromosomal gene mutation

Horizontal Gene transfer

22
Q

What is chromosomal gene mutation and how does it pre-dispose to development of AB resistant pop of bacteria?

A

o Chromosomal gene mutates in one bacteria in a population, conferring a resistance to antibiotic
o Antibiotic kills all other bacteria, acting as a selection pressure, giving resistant bacteria an advantage
o Population of antibiotic resistant bacteria daughter cells

23
Q

Give three types of horizontal gene transfer

A

Transformation
Transduction
Conjugation

24
Q

What is transformation?

A

o Bacteria with antibiotic resistance gene releases DNA

o Uptake of DNA by recipient cell, conferring antibiotic resistance

25
Q

What is transduction?

A

o Phage infected, antibiotic resistant Bacterial donor cell

o Phage passes the DNA conferring resistance to recipient cell

26
Q

What is conjugation?

A

o Connection is made between antibiotic resistant donor cell, and recipient cell
o Plasmid containing resistance gene is replicated and passes from donor cell to recipient cell
o Plasmid may even become incorporated into recipient cell DNA

27
Q

Give four methods of antibiotic resistance

A
  • Antibiotic Inactivation
  • Alteration of Drug Binding Site
  • Alteration of Metabolic Pathways
  • Reduced Intracellular Antibiotic Concentration
28
Q

What is antibiotic inactivation?

A

o Production of enzyme that inactivate the drug

 E.g. β-lactamase which inactivates Penicillins

29
Q

What is alteration of drug binding site?

A

o Modified binding sites so drugs no longer have affinity for them
 E.g. Bacterial ribosome alteration, meaning Aminoglycosides and Erythromycin cannot bind

30
Q

What is alteration of metabolic pathways?

A

o Development of altered metabolic pathways
 E.g. bacteria can become resistant to Trimethoprim due to acquired changes in their Dihydrofolate Redctase enzyme, which gives it very little affinity for the drug

31
Q

What is reduced intracellular antibiotic concentration?

A

o Active Efflux Mechanisms
 E.g. Active transport mechanisms used (e.g. p-glycoprotein) to pump a drug out of the bacterial cell because it accumulates to an effective level
o Decreased permeability
 E.g. Some bacteria become resistant to Tetracycline because they alter their cell membrane to make it impermeable to the drug

32
Q

Give three stages of the emergence of antibiotic resistnace

A
  1. Local selection (e.g. in a hospital)
  2. Clonal dissemination (e.g. around the country)
  3. Global spread
33
Q

Give five main antibiotic resistant bacteria

A

o Methicillin Resistant Staphylococcus Aureus (MRSA)
o Glycopeptide Intermediate susceptibility Staphylococcus Aureus (GISA)
o Glycopeptide Resistant Enterococci (GRE)
o Extended Spectrum Beta Lactamase enterobacteriaceae (ESBLs)
o Extensively Drug Resistant Klebsiella Pneumoniae (XDR-KP)

  • MDRTB
34
Q

Give four parts of anti-microbial stewardship

A

o Right antibiotic
o Right time
o Right dose, frequency and duration (Pharmacokinetics – ADME)
o Right route

35
Q

Give two stages of infection control

A

Prevent the spread of recognised resistant bacteria

Prevent bactrerial exposure to antiotics

36
Q

How can we prevent the spread of recognised resistant bacteria?

A

 Isolation or cohorting
 Hand hygiene
 Decolonisation of patients

37
Q

How can we prevent bacterial exposure to antibiotics?

A

 Minimise risk of infection

 Monitor and control antibiotic prescribing

38
Q

What are two different types of AB killing?

A

Time dependent killing
o Prolonged antibiotic presence at the site of infection, but not high concentration
Concentration dependent killing
o High antibiotic concentration at the site of infection, but short duration

39
Q

What is MIC?

A

Minimum Inhibitory Concentration – MIC
The MIC is the lowest concentration of an antibiotic that will inhibit the visible growth of a microorganism after overnight incubation.
A MIC is generally regarded as the most basic laboratory measurement of the activity of a microbial agent against an organism.