Lecture 3 Flashcards

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1
Q

What are 3 physical antimicrobial techniques used?

A

heat, radiation, and filtration

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2
Q

What are 3 chemical antimicrobial techniques used?

A

disinfectants, antisceptics, and antimicrobials

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3
Q

What are antibiotics?

A

a chemical substance produced by a bacterium that kills/inhibits the growth of another bacterium

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4
Q

What are antisceptics?

A

kills microbial cells but not eukaryotic cells

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5
Q

Which type of antimicrobial technique can damage eurkaryotic cells?

A

disinfectants

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6
Q

What does bacteriostatic mean?

A

inhibits growth of bacteria

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7
Q

What does bacteriocidal mean?

A

kills bacterium

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8
Q

What does bacteriolytic mean?

A

lyses bacterium

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9
Q

Who and when was penicillin discovered?

A

Alexander fleming, 1928

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10
Q

What year was penicillin started to be used medically?

A

1945

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11
Q

Who developed the concept of toxicity?

A

Paul Erlich

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12
Q

What was the cause in the increase of life expectancy between 1830 and 1900?

A

the Golden Age of Microbiology

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13
Q

What is sulfanilamide?

A

analog of PAD (component of folic acid)

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14
Q

How does sulfanilamide work at a molecular level?

A

inhibits fold acid synthesis (competitive inhibition) in bacteria

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15
Q

How do eukaryotic cells and bacterial cells get folic acid?

A

bacteria needs to make them because can’t uptake it, eukaryotic uptakes it from environment

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16
Q

What is the most common group of antibiotics?

A

cephalosporin and penicillin

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17
Q

What antibiotic group do cephalosporin and penicillin belong to?

A

beta-lactam antibiotics

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18
Q

What are the 3 things that limit the efficacy of antimicrobial drugs?

A

speed of action, sensitivity of target, side effects

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19
Q

In terms of speed of action, why do some antibiotics have a weaker or faster effect than other antibiotics?

A

availibility of target, location of target, and mode of taking the antibiotic or the body organ comes into play || pills take a longer time to take effect

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20
Q

What are broad-spectrum of antibiotics?

A

act on broad-spectrum type of targets bacterial species; ie: targets any bacteria with a glycine interbridge (= includes all gram+ species)

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21
Q

What are narrow-spectrum of antibiotics?

A

antibiotic that targets only one type of species

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22
Q

If you are a doctor prescribing a patient antibiotics without having much time to come up with a diagnostic, which type of antibiotic will you prescribe: broad or narrow?

A

broad = don’t know what specifically is going on

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23
Q

How are antibiotics selective?

A

only target prokaryotic cell and not eukaryotic cells

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24
Q

Which type of antibiotic is best used for an infection? Bacteriocidal or bacteriostatic and why?

A

depends on the situation but it is safer to use bacteriostatic for those pathogens that have endotoxins (if lysed = endotoxins are released)

25
Q

What is an example of antibiotic selectivity that reduces the pathogen’s toxicity to the host?

A

inhibiting metabolic that are only present in microbes

26
Q

What are 3 methods bacteria become resistant to antibiotics?

A

synthesis of an enzyme that breaks down antibitoic || prevent antibiotic from accessing target site || modification of the target site

27
Q

3 ways how bacteria can become resistant to antibiotics?

A

over-usage of an antibiotic or non-compliance; over-usage in agriculture; over prescription (use of antibiotics when no need to)

28
Q

How can non-compliance with a antibiotic medication lead to antibiotic resistance?

A

may not kill ALL pathogens inside = will create mutations against antibiotic and pass on that resistance gene via plasmids to other bacterium or new progeny

29
Q

What are the 3 main types of super-bugs?

A

Clostridium difficile, Neisseria gonnhorae, CP-resistent enterobacteriaceae

30
Q

What is clostridium difficile?

A

opportunistic pathogen found in healthy microbiota but with over-usage of antibiotics = kill other microbes = C.diff will take over and make you sick

31
Q

What are the 4 types of antibiotics?

A

B-lactam antibiotics, vancomycin, quinolones, antiribosomal antibiotics

32
Q

What are beta-lactam antibiotics?

A

consists of a beta-lactam ring structure where the variation happens at the n-acyl group

33
Q

What type of affect will beta-lactam antibiotics on a bacterial species? (bacteriostatic, bacteriolytic, or bacteriocidal)

A

bacteriocidal

34
Q

Which type of target sensitivity do beta-lactam antibiotics have?

A

broad-spectrum

35
Q

What is Penicillin G?

A

first antibiotic by FLeming, works better on Gram+ than on Gram–

36
Q

What are 3 examples of beta-lactam antibiotics?

A

penicillin, cephalosporins, cephamycins

37
Q

Why doesn’t penicillin work well with gram– bacteria?

A

outer-membrane doesn’t allow antibiotic to penetrate through it

38
Q

What type of penicillin-alternative is used for gram– bacteria?

A

ampicillin

39
Q

What is autolysin?

A

gene/protein that degrades peptidoglycan cell wall

40
Q

How can a penicillin be bacteriostatic?

A

If the bacteria doesn’t have the gene for autolysin = cell wall synthesis will only be affected

41
Q

Why is penicillin considered a bacteriocidal antibiotic?

A

inhibits penicillin-binding proteind (peptidases) new synthesis of cell wall and (if autolysin is present) begins to degrade current cell wall –> leads to bacterial cells to lyse

42
Q

What are beta-lactamases?

A

enzymes produced by pathogens that reduce permeability across outer-membrane = alters penicillin-binding proteins || breaks down b-lactam antibiotics

43
Q

What is vancomycin?

A

glycopeptide antibiotic

44
Q

What type of affect will vancomycin antibiotics on a bacterial species? (bacteriostatic, bacteriolytic, or bacteriocidal) How?

A

bacteriostatic = blocks synthesis of cell wall

45
Q

Why can’t you tale vancomycin orally?

A

protein-based = cannot take as a pill

46
Q

What does vancomyin target? In what type of bacteria and how?

A

D-alanine peptide blocks incorportation of another sugar chain onto growing polypeptide; only in gram+

47
Q

What is vancomycin used to treat?

A

MRSA infections

48
Q

How can we use protein-based antibiotics?

A

as a cream

49
Q

How does bacteria build up resistance to vancomycin?

A

alters peptide sequence in peptidoglycan so vancomycin doesn’t bind to it

50
Q

What are quinolones?

A

inhibit the action of bacterial DNA gyrase topoisomerase = breakdown of bacterial DNA

51
Q

What are topoisomerases?

A

makes DNA more compact

52
Q

What happens when you inhibit topoisomerase action?

A

cause DNA to breakdown

53
Q

What type of effect will quinolone antibiotics on a bacterial species? (bacteriostatic, bacteriolytic, or bacteriocidal) How?

A

bacteriolytic

54
Q

What are 2 ways bacteria can become resistant to quionolones?

A

change in topoisomerase or DNA gyrase or bacterium can develop a mechanism by removing antibiotic from the cytoplasm via efflux pump and pump it out into environment

55
Q

Which type of target sensitivity do anti-ribosomal antibiotics have?

A

broad-spectrum

56
Q

What are 3 examples of anti-ribosomal antibiotics?

A

tetracycline, erythromycin, streptomycin

57
Q

What do anti-ribosomal antibiotics bind to?

A

30S or 50S ribosomal subunit

58
Q

What are 3 methods bacterial species can be resistant to anti-ribosomal antibiotics?

A

reducing cell envelope permeability, modifying target, excretion of antibiotic from bacterial cytoplasm