Antibiotics Flashcards

1
Q

Antibiotic modes of action (3)

A
  1. Bacteriostatic
  2. Bacteriocidal
  3. Bacteriolytic
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2
Q

Bacteriostatic

A

Total cell count and viable cell count remain the same

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3
Q

Bacteriocidal

A

Total cell count remains the same but viable cell count decreases

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4
Q

Bacteriolytic

A

Total cell count and viable cell count both decrease

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5
Q

Cell wall synthesis ABs

A
Cycloserine
Penicillin
Carbapenems
Cephalosporins
Bacitracin
Vancomycin
Monobactams
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6
Q

Folic acid ABs

A

Trimethoprim

Sulfonamides

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7
Q

Cytoplasmic membrane structure ABs

A

Polymyxins

Daptomycin

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8
Q

Lipid biosynthesis ABs

A

Plantensymicin

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9
Q

Protein synthesis ABs (tRNA)

A

Mupirocin

Puromycin

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10
Q

30S inhibitors ABs

A
Tetracyclines
Spectinomycin
Streptomycin
Gentamycin
Kanamycin
Amikacin
Nitrofurans
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11
Q

50S inhibitors ABs

A

Erythromycin (macrolides)
Chloramphenicol
Clindamycin
Lincomycin

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12
Q

RNA polymerase ABs

A

Rifampin

Streptovaricins

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13
Q

RNA elongation ABs

A

Actinomycin

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14
Q

DNA gyrase ABs

A

Quinolones: Nalidixic acid, Ciprofloxacin, Novobiocin

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15
Q

Macrolide structure

A

12-16 membered macrolactone ring with various amino sugars

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16
Q

What do macrolides do

A

Inhibit the 50S subunit of the ribosome

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17
Q

In the 50s subunit

A

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

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18
Q

What effect does macrolide binding have

A

Inhibition of translation (peptides can’t exit tunnel)

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19
Q

What do fluoroquinolones do

A

Target DNA gyrase

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20
Q

Which kinds of DNA gyrase do fluoroquinolones target

A

Topoisomerase II and IV

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21
Q

Fluoroquinolones are particularly effective against

A

Gram positive bacteria

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22
Q

Fluoroquinolones enter Gram negative bacteria through

A

Outer membrane porins

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23
Q

Fluoroquinolones enter Gram positive bacteria by

A

Passive diffusion

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24
Q

Newer fluoroquinolones have a

A

Broader spectrum and better activity against Gram positive

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25
Fluoroquinolones are the
Second most used antibiotic
26
A synthetic antimicrobial
Fluoroquinolones
27
Fluoroquinones include
Nalidixic acid Ciprofloxacin Novobiocin
28
Cephalosporins are
Semi synthetic beta lactam antibiotics related to penicillin
29
Cephalosporins are derived from
Cephalosporium (fungus)
30
Beta lactam antibiotics interfere with
Bacterial cell wall synthesis
31
Peptidoglycan is made up of
alternating residues of β-(1,4) linked N-acetylglucosamine (NAG) and N-acetylmuramic acid (NAM)
32
Beta lactam antibiotics bind to
Transpeptidase enzymes that normally catalyze linkage of the glycan chains (where new tetrapeptides have been inserted) Binding stops this activity
33
New ABs inhibit
``` a broad range of targets including: topoisomerase protein synthesis cell membranes cell wall ```
34
Beta lactamase inhibitors
Overcome inactivation of beta lactam antibiotics
35
Phage are
Natural antimicrobials
36
Stages of phage infection (5)
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
Phage attachment is
Highly specific
38
Peptidoglycan and pore formation by lytic phage allows
Phage DNA injection
39
Phage late proteins include
Lysins, Holins, Murein synthesis inhibitors
40
Phage late proteins are responsible for
Host cell lysis
41
Lytic phage advantages
Cheap | Specific
42
Lytic phage disadvantages
Narrow spectrum | Rapid resistance
43
Alternative phage strategies use
Phage to deliver a protein that interferes with an essential bacterial process
44
Alternative phage strategies cause
Bacterial to be more susceptible to ABs
45
Phage therapy can be combined with
CRISPR
46
Anti Virulence Strategies
Inhibit specific mechanisms that promote infection
47
Anti virulence strategies offer
Reduced selection pressure for drug resistant mutation
48
Virulence specific drugs are good because
They do not cause the dramatic alteration in host microbiota that ABs do
49
UPEC
Uro pathogenic E.coli
50
Mechanism of UPEC infection (5)
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
IBC
Intracellular bacterial community
52
UPEC in anti virulence strategies (2)
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
Quorum sensing
Bacterial communication
54
Quorum sensing controls
A range of phenotypes including virulence factors
55
Inhibiting quorum sensing with a reporter upstream of a quorum sensing gene
Can result in virulence genes being switched off
56
Reporter genes can be used to monitor
The levels of expression of another gene
57
Targeting toxin production in anti virulence strategies
Toxin production is tightly regulated | Virstatin inhibits transcription of cholera toxin
58
Virstatin
Allows targeting of a specific operon that produces cholera toxin
59
Receptor mimics in anti virulence strategies
Mop up the toxin, stronger affinity so no binding to host receptor
60
Protein secretion systems in anti virulence
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
Faecal extracts inhibit the invasiveness of
Salmonella
62
The human gut metabolome
Has anti virulence activity
63
Type III secretion systems produce
Effectors that cause disease (actin rearrangment etc)
64
Synergistic drug usage causes problems because
Killing off susceptible bacteria removes competition and allows multi drug resistant bacteria to proliferate