Antibiotics Flashcards

You may prefer our related Brainscape-certified flashcards:
1
Q

Antibiotic modes of action (3)

A
  1. Bacteriostatic
  2. Bacteriocidal
  3. Bacteriolytic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Bacteriostatic

A

Total cell count and viable cell count remain the same

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Bacteriocidal

A

Total cell count remains the same but viable cell count decreases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Bacteriolytic

A

Total cell count and viable cell count both decrease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Cell wall synthesis ABs

A
Cycloserine
Penicillin
Carbapenems
Cephalosporins
Bacitracin
Vancomycin
Monobactams
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Folic acid ABs

A

Trimethoprim

Sulfonamides

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Cytoplasmic membrane structure ABs

A

Polymyxins

Daptomycin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Lipid biosynthesis ABs

A

Plantensymicin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Protein synthesis ABs (tRNA)

A

Mupirocin

Puromycin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

30S inhibitors ABs

A
Tetracyclines
Spectinomycin
Streptomycin
Gentamycin
Kanamycin
Amikacin
Nitrofurans
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

50S inhibitors ABs

A

Erythromycin (macrolides)
Chloramphenicol
Clindamycin
Lincomycin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

RNA polymerase ABs

A

Rifampin

Streptovaricins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

RNA elongation ABs

A

Actinomycin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

DNA gyrase ABs

A

Quinolones: Nalidixic acid, Ciprofloxacin, Novobiocin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Macrolide structure

A

12-16 membered macrolactone ring with various amino sugars

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What do macrolides do

A

Inhibit the 50S subunit of the ribosome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

In the 50s subunit

A

Macrolides bind to a specific site in the upper part of the peptide exit tunnel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What effect does macrolide binding have

A

Inhibition of translation (peptides can’t exit tunnel)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What do fluoroquinolones do

A

Target DNA gyrase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Which kinds of DNA gyrase do fluoroquinolones target

A

Topoisomerase II and IV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Fluoroquinolones are particularly effective against

A

Gram positive bacteria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Fluoroquinolones enter Gram negative bacteria through

A

Outer membrane porins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Fluoroquinolones enter Gram positive bacteria by

A

Passive diffusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Newer fluoroquinolones have a

A

Broader spectrum and better activity against Gram positive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Fluoroquinolones are the

A

Second most used antibiotic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

A synthetic antimicrobial

A

Fluoroquinolones

27
Q

Fluoroquinones include

A

Nalidixic acid
Ciprofloxacin
Novobiocin

28
Q

Cephalosporins are

A

Semi synthetic beta lactam antibiotics related to penicillin

29
Q

Cephalosporins are derived from

A

Cephalosporium (fungus)

30
Q

Beta lactam antibiotics interfere with

A

Bacterial cell wall synthesis

31
Q

Peptidoglycan is made up of

A

alternating residues of β-(1,4) linked N-acetylglucosamine (NAG) and N-acetylmuramic acid (NAM)

32
Q

Beta lactam antibiotics bind to

A

Transpeptidase enzymes that normally catalyze linkage of the glycan chains (where new tetrapeptides have been inserted)
Binding stops this activity

33
Q

New ABs inhibit

A
a broad range of targets including:
topoisomerase
protein synthesis
cell membranes 
cell wall
34
Q

Beta lactamase inhibitors

A

Overcome inactivation of beta lactam antibiotics

35
Q

Phage are

A

Natural antimicrobials

36
Q

Stages of phage infection (5)

A
  1. Adsorption to a specific receptor
  2. DNA injection
  3. Redirection of host metabolism to phage replication
  4. Assembly and packing of phage particles
  5. Bacterial cell lysis and progeny release
37
Q

Phage attachment is

A

Highly specific

38
Q

Peptidoglycan and pore formation by lytic phage allows

A

Phage DNA injection

39
Q

Phage late proteins include

A

Lysins, Holins, Murein synthesis inhibitors

40
Q

Phage late proteins are responsible for

A

Host cell lysis

41
Q

Lytic phage advantages

A

Cheap

Specific

42
Q

Lytic phage disadvantages

A

Narrow spectrum

Rapid resistance

43
Q

Alternative phage strategies use

A

Phage to deliver a protein that interferes with an essential bacterial process

44
Q

Alternative phage strategies cause

A

Bacterial to be more susceptible to ABs

45
Q

Phage therapy can be combined with

A

CRISPR

46
Q

Anti Virulence Strategies

A

Inhibit specific mechanisms that promote infection

47
Q

Anti virulence strategies offer

A

Reduced selection pressure for drug resistant mutation

48
Q

Virulence specific drugs are good because

A

They do not cause the dramatic alteration in host microbiota that ABs do

49
Q

UPEC

A

Uro pathogenic E.coli

50
Q

Mechanism of UPEC infection (5)

A
  1. Binding to Facet cells
  2. Invasion and replication in cells
  3. Biofilm formation (IBC)
  4. Biomass dispersion and cell exit
  5. Spread of infection
51
Q

IBC

A

Intracellular bacterial community

52
Q

UPEC in anti virulence strategies (2)

A
  1. Pilicides
    Pilus binds to uroplakin on facet cells - no pili=no binding
  2. Creation of analogs to interrupt mediation of binding to the natural receptor
53
Q

Quorum sensing

A

Bacterial communication

54
Q

Quorum sensing controls

A

A range of phenotypes including virulence factors

55
Q

Inhibiting quorum sensing with a reporter upstream of a quorum sensing gene

A

Can result in virulence genes being switched off

56
Q

Reporter genes can be used to monitor

A

The levels of expression of another gene

57
Q

Targeting toxin production in anti virulence strategies

A

Toxin production is tightly regulated

Virstatin inhibits transcription of cholera toxin

58
Q

Virstatin

A

Allows targeting of a specific operon that produces cholera toxin

59
Q

Receptor mimics in anti virulence strategies

A

Mop up the toxin, stronger affinity so no binding to host receptor

60
Q

Protein secretion systems in anti virulence

A

Bacteria need to get proteins to the cell wall
Molecular needles that inject effector molecules into host cell membranes
Very specific host cell pathogens
Knocking out secretion systems reduce virulence

61
Q

Faecal extracts inhibit the invasiveness of

A

Salmonella

62
Q

The human gut metabolome

A

Has anti virulence activity

63
Q

Type III secretion systems produce

A

Effectors that cause disease (actin rearrangment etc)

64
Q

Synergistic drug usage causes problems because

A

Killing off susceptible bacteria removes competition and allows multi drug resistant bacteria to proliferate