Micro Antibiotics Flashcards

1
Q

What lead to the discovery of antibiotics?

A

Poor aseptic technique

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2
Q

Who discovered the first penicillin?

A

Alexander Flemming

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3
Q

What is the definition of an antibiotic?

A

An antimicrobial chemcial that is naturally produced by microbes

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4
Q

What are two examples of natural antibiotics produced from bacteria?

A

Streptomyces and Bacillus

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5
Q

What are two examples of natural antibiotics produced from fungi?

A

Penicillium and Cephalosporium

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6
Q

What are two examples of an advantage for bacteria that make antibiotics?

A

The antibiotic can act as a cell to cell signaling molecule, and they may be able to kill off their neighbors as competition

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7
Q

What are some other uses for antibiotics beyond treating human infections?

A

Supplements in animal fed, vet medicine

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8
Q

What are the three kinds of antibiotics?

A
  1. Natural
  2. Synthetic
  3. Semisynthetic
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9
Q

What is a synthetic antibiotic?

A

It is totally chemically created in a lab

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10
Q

What is a semisynthetic antibiotic?

A

It is a derivative of a naturally produced antibiotic that has been structurally changed to create a better working drug

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11
Q

What are some characteristics that make up a better drug?

A
  1. Nontoxic to human cells
  2. Broader spectrum
  3. Can be given orally or by IV
  4. High half life in humans (it’s not degraded quickly)
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12
Q

What does selectively toxic mean?

A

That the antibiotic is more toxic to one cell (the target cell) than another (human cells)

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13
Q

What are the two classifications of antibiotics that described how they effect infections?

A
  1. Bacteriostatic

2. Bacteriocidal

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14
Q

What is bacteriostatic?

A

The antibiotic inhibits growth of the infectious cells, and therefore limits the amount of cells the immune system has to fight

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15
Q

What is bacteriocidal?

A

The antibiotic kills the infectious cells

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16
Q

Which is more common, bacteriostatic or bacteriocidal antibiotics?

A

Bacteriostatic

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17
Q

What are half the antibiotics in the US used for?

A

Animal feed

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18
Q

What are two reasons we put antibiotics in animal feed?

A
  1. Prophylactic - it prevents the animals from being infected
  2. It makes the animals grow faster, because it decreases the bacteria in the body’s normal flora and therefore more nutrients can be absorbed by the animal
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19
Q

What is a broad spectrum?

A

The antibiotic affects multiple groups of microbes

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20
Q

What is a narrow spectrum?

A

The antibiotic affects only a few groups of microbes

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21
Q

Are natural (first generation) penicillins broad or narrow spectrum?

A

Narrow, they couldn’t pass the outer membrane of gram negative bacteria

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22
Q

Are semisynthetic (second generation) penicillins broad or narrow spectrum?

A

Broader, could affect more groups of bacteria

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23
Q

What is an example of a second generation penicillin?

A

Methicillin

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24
Q

What are two ways that antibiotics are selectively toxic?

A
  1. They target structures that our cells lack

2. They target structures that we have but the bacteria has a different shaped structure

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25
Q

What are the five targets of antibiotics?

A
  1. Inhibition of cell wall synthesis
  2. Inhibition of protein synthesis
  3. Inhibition of nucleic acid replication and transcription
  4. Injury to the plasma membrane
  5. Inhibition of synthesis of essential metabolites
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26
Q

If an antibiotics is targeting cell wall synthesis, what structure is it specifically targeting?

A

Peptidoglycan

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27
Q

What two antibiotic groups target peptidoglycan?

A
  1. Beta lactam drugs

2. Vancomycin

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28
Q

What are three examples of beta lactam drugs?

A
  1. Penicillin
  2. Cephalosporin
  3. Carbapenem
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29
Q

What do beta lactam drugs have that help them to function?

A

The beta lactam ring

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30
Q

Why might beta lactam drugs not work? What do we give the patient then instead?

A

They bacteria could be resistant or the patient could be allergic. We would then use the “drug of last resort,” Vancomycin

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31
Q

How does vancomycin work in comparison to beta lactam drugs?

A

They both inhibit the same enzyme but they do it in different ways

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32
Q

Why don’t we prescribe vancomycin more often?

A
  1. We don’t want to develop bacteria resistance
  2. It is more expensive
  3. It needs to be given through IV
  4. It has bad side effects
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33
Q

What enzyme is inhibited by beta lactam and vancomycin?

A

Transpeptidase

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34
Q

What happens to the bacteria that are effected by beta lactam drugs and vancomycin?

A

Osmotic lysis of actively growing bacteria

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35
Q

Why aren’t beta lactam drugs and vancomycin toxic to human cells?

A

Our cells don’t produce transpeptidase

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36
Q

What is transpeptidase also known as?

A

Penicillin binding protein

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37
Q

What does transpeptidase do?

A

It catalyzes the cross link formation in peptidoglycan

38
Q

How do beta lactam drugs inhibit transpeptidase?

A

They bind to transpeptidase so that the enzyme can’t cross link the NAM sugars between strands of peptidoglycan

39
Q

What happens to the bacterial cells when they can’t cross link their peptidoglycan?

A

They still grow and divide but half of their peptidoglycan is not structurally sound so eventually the daughter cells will burst from osmotic pressure

40
Q

What kind of antibiotics inhibit protein synthesis?

A

Z pack (azithromycin)

41
Q

How does the Z pack inhibit protein synthesis?

A

It inhibits the bacterial ribosome and translation

42
Q

What specifically do antibiotics do when they are inhibiting nucleic acid synthesis?

A

Either inhibiting DNA gyrase or RNA polymerase

43
Q

What is another name for DNA gyrase?

A

Topoisomerase

44
Q

What does DNA gyrase/topoisomerase do?

A

It releives the tension (supercoils) in the DNA strands during replication that result from replication bubbles

45
Q

What happens when DNA gyrase is inhibited?

A

DNA replication stops

46
Q

What kinds of antibiotics inhibit DNA gyrase?

A

Quinolones, fluoroquinolones,

47
Q

What is a specific example of a quinolone?

A

Ciprofloxacin

48
Q

What are antimetabolites?

A

Antibiotics that inhibit metabolic pathways that are not present in humans

49
Q

What kind of inhibitor does the antibiotic act as when it inhibits metabolic pathways? Why?

A

Competitive inhibitor, because it attaches to the enzymes active site so that the substrates can’t bind and the pathway does not occur

50
Q

What is an example of a metabolic pathway that might be targeted by an antibiotic?

A

The folic acid pathway, because only bacteria can make folic acid, humans do not have the pathway

51
Q

What do bacteria need folic acid for?

A

To synthesize DNA and RNA nucleotides

52
Q

What are two examples of antibiotics that inhibit metabolic pathways?

A

Trimethoprim and sulfa drugs

53
Q

What do antibiotics do to the bacteria if they cause cell membrane damage?

A

They either cause an increase in the permeability of the membrane or inhibit fatty acid synthesis

54
Q

What is the unique target of antifungal drugs that cause cell membrane damage?

A

Ergosterol

55
Q

Why do bacterial drugs that cause cell membrane damage tend to be topical?

A

Because they are not very selectively toxic because the cell membranes of prokaryotes are very similar to eukaryotes (they are too toxic to be given internally, we can put them on the skin because our top layers of skin are dead anyways)

56
Q

What are three issues with safety and side effects of antibiotics?

A
  1. Toxicity
  2. Allergies
  3. Disruption of the normal flora can cause a superinfection
57
Q

Which patients typically get superinfections?

A

Those that have been on several different antibiotics at once for an extended period of time

58
Q

How does a superinfection occur?

A

It is a secondary infection caused by antibiotic therapy. There is an overgrowth of resistant pathogens that may be part of the normal flora, but because there are less bacteria to compete with, these pathogens grow to numbers that cause symptoms.

59
Q

What are two organisms that typically cause superinfections?

A
  1. Candida albicans - causes candidasis

2. Clostridium difficile - causes pseudomembranous colitis

60
Q

Why is pseudomembranous colitis so hard to get rid of?

A

Clostridium difficile can turn into an endospore

61
Q

What is a treatment for pseudomembranous colitis?

A

A fecal transplant to restore the numbers of good bacteria in your normal flora

62
Q

Why are there so many cases of antibiotic resistance today?

A
  1. Antibiotics are overused and over prescribed

2. Antibiotics are used in animal feed, causing selective pressure for drug resistant strains

63
Q

What is a common overuse of antimicrobial solutions? What is the name of the specific agent?

A

Antimicrobial soap (triclosan), this was originally only used in hospitals with sick people, now it is found in baby toys, garbage bags, etc. Increased use leads to increased resistance

64
Q

What are two ways that bacteria can acquire anitbiotic resistant genes?

A
  1. Mutations occur

2. They acquire genes from an existing bacteria - horizontal gene transfer

65
Q

What are three kinds of horizontal gene transfer?

A
  1. Conjugation
  2. Transformation
  3. Transduction
66
Q

What is conjugation?

A

There is a transfer of a plasmid copy from the donor to the recipient

67
Q

What is required for conjugation to occur?

A

Direct cell to cell contract

68
Q

What kinds of plasmids are able to be transferred through conjugation? What is the name of a specific plasmid?

A

Only conjugative plasmids can be transferred using conjugation. For example, the F plasmid or F factor

69
Q

What is the F factor?

A

An E. coli plasmid that is the most studied

70
Q

What genes does the F plasmid have that are required for conjugation?

A

Sex pilus proteins

Proteins that initiate cell to cell contact

71
Q

How many origins of replication does the F plasmid have? What are they?

A

Two - OriV and OriT

72
Q

What is the OriV origin of replication?

A

the origin for standard replication

73
Q

What is the OriT origin of replication?

A

The origin for replication during DNA transfer

74
Q

What is another name for the donor and recipient cells in conjugation?

A

F+ is the donor and F- is the recipient

75
Q

What are the steps to conjugation?

A
  1. The donor’s sex pilus attaches to the recipient
  2. Pilus contracts and cells attach
  3. One strand is broken at OriT, 5’ end enters the recipient (relaxosome)
  4. Complementary strands synthesized in both recipient and donor
  5. Recipient is now an F+ cell
76
Q

What is transformation?

A

The uptake by livings cells of free floating DNA from dead, lysed cells

77
Q

What does competent mean?

A

The cell has the ability to take up DNA from the environment

78
Q

What is natural competence?

A

Certain bacteria have a specific protein that transports DNA across the cell envelope

79
Q

What is lab induced competence?

A

For bacteria that don’t produce the proper transporter, the lab increases the membrane permeability

80
Q

What three things does the lab use to alter membrane permeability in lab induced competence?

A
  1. Heat
  2. Calcium
  3. Electricity
81
Q

What kind of DNA is transferred during transformation?

A

Any kind

82
Q

Do cells have to be touching to use transformation?

A

No

83
Q

What is transduction?

A

The transfer of genes from one organism to another by a virus

84
Q

What is generalized transduction?

A

Any part of the bacterial genome can be transferred

85
Q

What are the steps of transduction?

A
  1. A phage infects the donor bacterial cell
  2. Phage DNA and proteins are made and the bacterial chromosome is broken down into pieces
  3. Sometimes pieces of bacterial DNA are packaged in a phage capsid, then the donor lyses and releases this phage
  4. A phage carrying bacterial DNA infects a new host cell (recipient)
  5. Recombination can occur, producing a recombinant cell with a genotype different from both the donor and recipient cells
86
Q

What is target focused resistance?

A

A way that bacteria develop resistance to drugs - they modify the target of the antibiotic and replace it with a version that is resistant to the drug

87
Q

What are four examples of mechanisms of antibiotic resistance?

A
  1. Block entry
  2. Inactivating enzymes
  3. Alteration of target molecule
  4. Efflux of antibiotic
88
Q

What is drug focused resistance?

A
  1. It prevents the uptake of an antibiotic into the cell
  2. Converts it from an active form to an inactive form
  3. Pumps antibiotic out of the cell**
89
Q

How does the bacteria know how to be drug focused resistant?

A

The trait is encoded by resistance genes present in the chromosome or on the plasmid

90
Q

How can heath care professionals limit the spread of antibiotic resistance?

A
  1. Encourage and educate about vaccinations
  2. Wash hands
  3. Prescribe only when necessary
  4. Isolate patients infected with multiple drug resistant pathogens
91
Q

How can patients limit the spread of antibiotic resistance?

A
  1. Be up to date on vaccinations
  2. Do not demand or request antibiotics
  3. Limit the use of antimicrobial products
  4. Do not stockpile unused antibiotics
  5. Follow instructions exactly and do not stop use just because you feel better