Lecture 3 - Antibiotics & Resistance Flashcards

1
Q

Disinfectants

A

For inanimate objects

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2
Q

Antiseptics

A

nontoxic, for living tissues (hand san)

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3
Q

Antibiotics

A

antimicrobials from bacteria and fungi exploited by humans

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4
Q

How was penicillin discovered

A

Was on a plate withs staph, and no growth around the penicillin

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5
Q

Best way to kill bacteria

A

Antibiotics

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6
Q

When are antibiotics absolutely required?

A

Surgery and essentially all forms of medicine

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7
Q

2 problems for antibiotics

A

No profit, less interest. Resistance always occurs

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8
Q

What are the 2 fates of antibiotics

A

Kill the bacteria or stunt the growth

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9
Q

MIC

A

Minimum inhibitory concentration - how much antibiotic is needed to stop growth

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10
Q

How do we test MIC

A

Various test tubes with varying conc and the bacteria. Which everyone shows a visible change is the MIC. NEW: strips used on plate with different antibiotics, as the strip moves towards to centre concentrate increases. Measure conc where growth of bacteria stops

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11
Q

5 Antibiotic Targets

A
  • cell wall synthesis
  • protein synthesis
  • DNA/RNA synthesis
  • folate synthesis
  • changes in cell membrane
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12
Q

How is cell wall synthesis stopped?

A
  • Using B-lactam rings that will bind to penicillin binding proteins (PBP) and will stop the cross linking
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13
Q

How does bacteria counteract b-lactam

A

Production of b-lactamase which destroys the lactam ring and thus no binding to peptide

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14
Q

What is used when penicillin resistance occurs?

A

Methicillin, can’t be cleaved by lactamase

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15
Q

How does the bacteria counteract methicillin?

A

Makes different Protein Binding Penicillin which won’t bind lactam or methicillin

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16
Q

What is the main job of Vancomycin

A

Stops cell wall synthesis for gram positives (can’t get through the outer membrane of g-)

17
Q

How does vancomycin work?

A

Binds the terminal d-ala-d-ala and stops transcription

18
Q

How does bacteria counteract vancomycin?

A

Changes terminal end to d-ala-d-lac so that vancomycin cannot bind

19
Q

What is the target for protein synthesis inhibition?

A

THE RIBOSOMES

20
Q

What is used to inhibit folic acid synthesis

A

Trimethoprim and sulfonamides

21
Q

Where is Folic Acid obtained from

A

Humans - diet, Bacteria - must synthesize on won

22
Q

What is used to inhibit DNA/RNA synthesis?

A

Fluoroquinolones which stop the coiling, and Rifampicin which stop RNA polymerase from working

23
Q

What is used to alter the cell membrane?

A

Polymyxin B, binds to LPS and disrupts the membrane

24
Q

What is horizontal transfer?

A

The gain of new genes from another organisms

25
Q

What are the 3 methods of horizontal gene transfer?

A

Transformation - floating dna
Transduction - bacteriophage
Conjugation - direct passing of plasmid

26
Q

Enterococci (VRE)

A

G+ cocci

27
Q

What does enterococci infect?

A

The GI tract

28
Q

What type of pathogen is Enterococci

A

Nosocomial pathogen

29
Q

Enterococci causes?

A

UTI, Surgical infections and endocarditis

30
Q

VRE stands for

A

Vancomycin resistant enterocci

31
Q

Acinetobacter baumannil

A

G-, nosocomial, very resistant to all antibiotics

32
Q

Klebsiella penumoniae

A

G-, nosocomial, pneumonia, highly resistnat

33
Q

Costridia

A

G+ rod shapped, forms endospores

34
Q

Clastridium difficile (C. diff) causes

A

pseudomembranous colitis - antibiotic caused diarrhea

35
Q

How is C. diff transmitted?

A

Via the focal oral route

36
Q

Toxins released by C. diff

A

A-B toxins, active and binding