S4 L1 - Antimicrobials and Resistance Flashcards

1
Q

4 types of Anti-microbials

How are Anti-bacterials classified?

How to choose the right antibiotic?

A

4 types of Anti-microbials:
•Antibacterial agents* – e.g. Penicillin (streptococci)
•Antifungal agents – e.g. Fluconazole (candida)
•Antiviral agents – e.g. Aciclovir (herpes simplex)
•Antiprotozoal agents – e.g. Metronidazole (trichomoniasis)

  • *Antibacterial agents (antibiotics) can be classified as follows:**
  • Bactericidal (kill bacteria) or Bacteriostatic (stop bacteria replicating and immune system takes care of them)
  • Spectrum – ‘broad’ v. ‘narrow’
  • Target site (mechanism of action) – e.g. cell wall, folate synthesis - see part 2
  • Chemical structure (antibacterial class) – e.g. ß lactams

Choosing the right antibiotic:
• Is it active against target organism?
• Does it reach the site of infection?
• Is it available in the right formulation (IV vs oral)?
• What is the half life (decides dosing frequency)?
• Does it interact with other drugs?
• Is there toxicity issues?
• Does it require therapeutic drug monitoring?
• Does your patient have an allergy to any antibiotic class

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2
Q

Measuring antibiotic activity
3 ways

A
  1. Disc sensitivity testing
  2. Minimum Inhibitory Concentration
  3. MIC - Epsilometer test (E-test)
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3
Q

Types of Antibiotic Resistance
3 and explain them

A

1) Intrinsic
– Either no target or access for the drug
– Usually permanent
E.g. bacterial species is naturally resistant to a certain antimicrobial – gram negative bacteria are often resistant to any antibiotics which target the peptidoglycan layer because they have an extra outer membrane

2) Acquired Spontaneously mutates
– acquires new genetic material or mutates
– Usually permanent
E.g. microbes become resistant to a certain antimicrobial through several mechanisms such as gene mutation or gene transfer.

3) Adaptive Linked to antibiotic resistance
– The organism responds to a stress (e.g. sub inhibitory level of antibiotic/antiviral/antifungal/antiparasitic)
E.g. the sub inhibitory levels induce the bacteria to switch on genes which confer resistance

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4
Q

Mechanism of Resistance
3 ways and explain

A

1) Enzymatic modification or destruction of antibiotics e.g. beta lactamase, an enzyme produced by Staphylococcus aureus, inactivates ß-lactam antibiotics - gets a mutation that helps destroy the antibiotic

2) Enzymatic alteration of antibiotic targets - Alter the target so the antibiotic can’t bind to it

3) Overexpression of efflux pumps - this pumps to antibiotics out

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5
Q

2 ways of more bacteria having this resistance

A
  1. Chromosome gene mutation - one bacteria carrying mutation which confers resistance multiples
  2. Horizontal gene transfer - Bacteria develop pilus. This allows the transfer of plasmid that has the resistance mutation to transfer from one bacteria to another. The plasmids can replicate. Both are now resistant.
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6
Q

Antimicrobials
THIS IS NOT IN MUCH DETAIL, JUST THE COVERING THE MOST IMPORTANT BITS- See folder to get indepth notes on this

A
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7
Q

Antibiotics:
- Inhibit cell wall synthesis
4 in one group
1 seperate

A
  • Beta-lactams: 4 sub-groups
  • Penicillin e.g. Amoxicillin, flucloxacillin, co-amoxiclav
  • Cephalosporins (4 generations of these) e.g. from 3rd generation is Ceftriaxone
  • Carbapenems e.g. Meropenem
  • Monobactams
  • Glycopeptides e.g. Vancomycin
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8
Q
  • *Note about:**
  • Cephalosporins
  • Meropenem
  • Vancomycin
A

- Cephalosporins: Concerns that they may cause C.diff infections (Cephalosporins can eliminate some of the natural gut flora, reducing competing for commensal in the gut microbiome including C.diff)

- Meropenem: Usually prescribe this if someone has a penicillin allergy (as it has a similar structure to penicillin’s)

- Vancomycin: Last resort drug as MRSA and C.diff aren’t resistant to it, so only given when absolutely necessary. Vancomycin is normally given IV (especially for systemic infections) as it can’t be absorbed via the gut. The exception to this is C.diff infections, it is given orally for these to target the GI tract.

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9
Q
  • *Anbiotics:**
  • Inhibit protein synthesis
  • 3 types
A

TAM

  • Tetracyclines e.g. Doxycycline
  • Aminoglycosides e.g. Gentamicin
  • Macrolides e.g. Erythromycin, Azithromycin, Clarithromycin
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10
Q
  • *Note about:**
  • Tetracycline
  • Gentamicin
A
  • *- Tetracyclines:** Can’t be given to children under 12, as it yellows teeth. Good choice if patient has a penicillin allergy.
  • *- Gentamicin:** Nephrotoxic and ototoxicity (damage to the ear)
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11
Q

Antibiotics
- Inhibit nucleic acid synthesis
1 group

A

- Quinolones e.g. Ciprofloxacin

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12
Q
  • *Antibiotics**
  • Inhibits folic acid synthesis
A
  • Trimethoprim
  • Sulphonamide
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13
Q
  • *Anti-Fungals**
  • 2 groups and what is there mechanism?
A

Two groups: Azoles and Polyenes

  • *Azoles:** e.g. Fluconazole – Inhibits cell wall synthesis and growth
  • *Polyenes:** e.g. Nystatin, Amphotericin – Inhibits cell membrane functions
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14
Q
  • *Anti-Virals**
  • 2 groups
A

ANTI-VIRALS:
Aciclovir
– Inhibits viral DNA polymerase
Tamiflu (Oseltamivir) – Inhibits neuraminidase

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