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Microbes and You > Antibiotic Resistance L12 L13 > Flashcards

Antibiotic Resistance L12 L13 Flashcards

1
Q

what is a disinfectant

A

broad range chemicals that are typically used on inert surfaces

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2
Q

do disinfectants kill all bacteria

A

may not kill all the bacteria on the surface, but will cause a significant reduction in the number of viable bacteria

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3
Q

are disinfectants used with humans in medical nature

A

may cause damage to human cells, so are not used as medical treatments for infection

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4
Q

what are antiseptics

A

also tend to be broad-range, killing a variety of different bacteria

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5
Q

do antiseptics harm humans

A

do not cause damage to human cells and tissues, so are typically used as topical treatments to prevent or treat infections

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6
Q

typical examples of antiseptics

A

mouthwash and iodine, which is used to cleanse the skin before surgery

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7
Q

what are antibiotics

A 
chemicals designed to only target microorganisms
microbial products (and their derivatives) that kill or inhibit the growth of susceptible micro-organisms
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8
Q

what ability do antibiotics typically have

A

ability to penetrate through human tissue without causing damage, and are used to treat internal infections

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9
Q

what are antibiotics used for

A

treat bacterial infection

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10
Q

who discovered first antibiotic

A

1928
alexander flemming
penicillium notum

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11
Q

what does penicillium notum do

A

inhibits growth of Staphylococcus aureus

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12
Q

in 1940 what happened to penicillin

A

was purified by Howard Florey and Ernst Chain and showed in vivo activity in mice infected with streptococci or staphylococci

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13
Q

what are the five main groups of targeted processes

A
  • Cell Wall Synthesis Inhibition
  • Protein Synthesis Inhibition
  • Nucleic Acid Synthesis Inhibition
  • Cell Membrane Disruption
  • Antimetabolites
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14
Q

what are the two main primary effects of antibiotics

A

bactericidal

bacteriostatic

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15
Q

what is bactericidal

A

these antibiotics cause death of the bacteria

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16
Q

what is bacteriostatic

A

these arrest the growth of the bacteria, but do not actually kill the bacteria

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17
Q

what happens to bacteria when bactericidal agent added

A

bacteria die

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18
Q

what happens to bacteria when bacteriostatic agent added

A

bacteria will stop growing

still survive, but inhibit their replication

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19
Q

what is the problem with antibiotics

A

Short time in resistance occurring in antibiotics created

Very quickly after use in clinic see resistance arise

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20
Q

how do we test for antibiotic resistance

A 
several tests used testing resistance/sensitivity of bacteria to different antibiotics
three most-commonly used are:
- E-test
- disk diffusion tests
- dilution susceptibility tests
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21
Q

what is MIC

A

Minimal Inhibitory Concentration

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22
Q

what is minimal inhibitory concentration

A

minimum concentration of an antibiotic needed to inhibit growth of an organism

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23
Q

what does the E-test allow

A

Allows resistance/susceptibility of a bacterial isolate to be tested along with determination of the MIC

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24
Q

what happens in the E-test

A

plate certain concentration of bacteria evenly across plates and impregnated E-test strips placed on top
plates are incubated overnight
gradient of antibiotic spreads into agar plate, inhibiting bacteria growth when at high enough concentrations

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25
Q

how can the E-test MIC be read

A

read as the point at which interface between the growth and no-growth zones crosses E-test strip

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26
Q

what are E-test strips

A

Uses a strip that is impregnated with bacteria testing, concentration gets lower as go down

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27
Q

what is similar to the E-test

A

Kirby-Bauer disk diffusion assay

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28
Q

what does the Kirby-Bauer disk diffusion assay determine

A

only resistance / susceptibility can be determined

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29
Q

what does the Kirby-Bauer disk diffusion assay not determine

A

MIC

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30
Q

what happens in Kirby-Bauer disk diffusion assay

A

Disks containing antibiotics tested, placed on plate spread with bacteria to be tested
zones of inhibition form around disks containing antibiotics to which the bacteria are susceptible

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31
Q

how is it determined if antibiotic is resistant in Kirby-Bauer disk diffusion assay

A

diameter of the zone of inhibition will be measured and compared to a standardised table which allows the determination of whether the bacteria are resistant, susceptible or intermediate

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32
Q

what does the dilution susceptibility tests look at

A

test looks at the growth of planktonic (free floating in liquid) bacteria in a range of concentrations of an antibiotic

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33
Q

what happens in dilution susceptibility tests

A

set of tubes are set up with growth media containing antibiotic at a range of concentrations
each inoculated with bacterium of interest
incubated overnight
growth checked

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34
Q

how is the MIC found in dilution susceptibility tests

A

lowest concentration of antibiotic that inhibited growth is determined – MIC of organism with that antibiotic

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35
Q

what are the three major types of antibiotics that target cell wall synthesis

A

1) Penicillins
2) Cephalosporins
3) Vancomycin

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36
Q

what are the two different mechanisms of antibiotics targeting cell wall synthesis

A

inhibiting actions of enzymes needed for production of peptidoglycan or by activating cell wall lytic enzymes

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37
Q

examples of bactericidal antibiotics

A

Penicillins
Cephalosporins
Vancomycin

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38
Q

how do penicillins vary

A

different penicillins have a side chain attached to the amino group, this varies between different penicillins

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39
Q

what is essential for penicillins activity

A

β-lactam ring is essential

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40
Q

what happens if β-lactam ring is cut

A

antibiotic doesn’t work

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41
Q

how have natural penicillins been allowed

A

penicillins vary in their side chains
has allowed natural penicillins to be modified and adapted for increasing stability / resistance to bacterial resistance mechanisms

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42
Q

examples of natural penicillins

A

Penicillin G and Penicillin V

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43
Q

how is penicillin G given

A

injection as it is susceptible to stomach acid degradation

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44
Q

how is penicillin V given

A

can be given orally as it is more acid-resistant

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45
Q

which penicillin is more acid stable

A

penicillin V is more acid stable as can resist acid, better for oral consumption as can resist the stomach acid

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46
Q

what are semisynthetic penicillins designed for

A

designed and engineered to either have a broader spectrum of activity (work against a wider group of bacteria) or to work against organisms that are resistant to natural penicillins

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47
Q

what is the mechanism of action for penicillin

A

binds to the transpeptidase
enzyme that cleaves final D-Ala from peptidoglycan monomer
blocking it from acting, inhibiting formation of peptidoglycan cross-links

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48
Q

what does the structure of penicillin resemble

A

the D-Ala-D-Ala structure found in peptidoglycan

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49
Q

what are β-lactamases

A

enzymes that hydrolyse a bond in the β-lactam ring

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50
Q

what are penicillinases

A

enzyme

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51
Q

where are β-lactamases found

A

chromosome and on plasmids in many bacterial species

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52
Q

what are ESBLs

A

Extended-spectrum β-lactamases

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53
Q

what do some ESBLs do

A

Some ESBL will cut penicillin and other things that have beta-lactam ring

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54
Q

what is NDM-1

A

name given to a newly-described class of beta-lactamases – ‘New Delhi Metallo-beta-lactamase-1’

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55
Q

what does NDM-1 confer

A

confers resistance to all beta-lactam antibiotics in use as well as carbapenems

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56
Q

examples of organisms are found to carry NDM-1 gene

A

E. coli

Salmonella

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57
Q

where is NDM-1 transfer

A

NDM-1 can rapidly transfer between bacterial species as it is often plasmid encoded

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58
Q

where are NDM-1 found

A

often found within transposons
plasmids
often found on plasmids containing other resistance genes, including other beta-lactamases, carbapenamases, genes for resistance to quinolones and aminoglycosides

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59
Q

what is the NDM-1 host range

A

also have a broad host range meaning they can replicate within a wide variety of bacterial species aiding in the spread of resistance

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60
Q

how are NMD-1 horizontally transferred

A

found within Transposons, giving it yet another way to be horizontally transferred between strains and species

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61
Q

what are carbapenems

A

members of beta-lactam group of antibiotics, they also contain beta-lactam ring

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62
Q

where are carbapenems originally isolated from

A

Streptomyces cattleya, but have been semisynthetic ones have been developed

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63
Q

what is carbapenems function

A

inhibiting cell wall synthesis

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64
Q

how do carbapenemases act

A

act to hydrolyse beta-lactam rings
most recognise almost all hydrolysable beta-lactams
working against penicillins and cephalosporins

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65
Q

where are KPC

A

found on transferable plasmids, predominantly in K. pneumoniae but now reported in other species such as Enterobacter and Salmonella

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66
Q

what antibiotic has emerging resistance mechanism

A

KPC

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67
Q

what are KPCs responsible for

A

almost 90% of carbapenem-resistant Klebsiella in several European countries

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68
Q

what does KPC cause

A

nosocomial pathogen affect severely ill and increase chances of patient mortality

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69
Q

what are treatment options for Klebsiella

A

limited, often resorting to use of Polymyxin B and Colistin

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70
Q

where are cephalosporins originally isolated from

A

fungus Cephalosporium

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71
Q

what do cephalosporins contain

A

β-lactam ring

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72
Q

what do cephalosporins do

A

Act to inhibit the formation of peptidoglycan cross-links similarly to penicillins

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73
Q

what are cephalosporins susceptible to

A

activity of β-lactamases

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74
Q

what produces vanomycin

A

bacterium Streptomyces orientalis

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75
Q

what is vanomycin structure

A

consists of a peptide linked to a disaccharide

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76
Q

what does vanomycin bind to

A

binds to the D-Ala-D-Ala residues at the end of peptidoglycan molecules

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77
Q

what is the effect of vanomycin binding to D-Ala-D-Ala

A

preventing transpeptidase from cleaving bond between them

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78
Q

how can vancomycin become resistance

A

Resistance to Vancomycin can occur if bacteria change terminal D-Ala residue into either a D-lactate or D-serine residue (Vancomycin can no longer bind, and the transpeptidase can still act to cleave the bond)

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79
Q

what is staphylococcus aureus

A

usually a commensal bacterium

opportunistic pathogen

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80
Q

where is staphylococcus aureus found

A

found on the skin and in the nasal cavity

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81
Q

when does staphylococcus aureus cause infection

A

enters into wounds, bloodstream

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82
Q

what is staphylococcus aureus treated

A

Originally treated using the penicillin-like drug Methicillin

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83
Q

what is staphylococcus aureus resistant to, effect

A

Resistance to methicillin arose – leading to the ‘superbug’ MRSA (Methicillin-Resistant Staphylococcus aureus)

84
Q

what is VRSA

A

Vancomycin Resistant Staphylococcus aureus

85
Q

what stops vanomycin binding - VRSA

A

VRSA strains have altered pentapeptides in their peptidoglycan which stops the Vancomycin from binding and acting

86
Q

where does vanomycin normally bind

A

to D-Ala-D-Ala,

87
Q

effect of vanomycin binding

A

inhibiting cell wall synthesis

88
Q

effect of VRSA strains not being able to bind

A

allowing the cells to maintain wall synthesis and survive treatment

89
Q

what does the VISA strain retain

A

the D-ala-D-ala residues at the end of the peptidoglycan chains

90
Q

what is VISA

A

Vancomycin Intermediate-resistant Staphylococcus aureus

91
Q

what does VISA do

A

show an increase thickness of cell wall – in S. aureus (Gram positive) cell wall is made of peptidoglycan

92
Q

what is the effect of VISA

A

increased peptidoglycan amount

Vancomycin cant reach cytoplasmic membrane where it acts on the peptidoglycan being made

93
Q

when do VISA strains lose thickened cell walls

A

lose their thickened cell walls when repeatedly cultured in absence of Vancomycin and MIC of cells also drops

94
Q

superbug examples

A

MRSA

VRSA

95
Q

what are the resistance mechanisms

A 
enzymatic inactivation
enzymatic addition
impermeability 
efflux
alternative pathway
altered target
96
Q

enzymatic inactivation example

A

beta-lactamases cut part of antibiotic

97
Q

enzymatic addition example

A

aminoglycosides

98
Q

impermeability example

A

beta-lactams

Bacteria can adapt their membranes Don’t allow antibiotic through to encounter enzymes etc

99
Q

efflux examples

A

tetracyclines

100
Q

alternative pathway examples

A

MRSA mecA

101
Q

altered target examples

A

rifampicin

102
Q

what are efflux pumps

A

pump out antibiotic before it has time to work

103
Q

what happens in rifampicin

A

alteration of binding site

104
Q

what happens in MRSA mecA

A

alternative pathway taken

bacteria can apply a different type protein to which the antibiotic wont bind to but will do the same job

105
Q

what happens in addition resistance

A

add molecules onto antibiotic e.g. phosphorylate

106
Q

how can resistance be transferred

A

transformation
conjugation
transposons

107
Q

what happens in transformation resistance transformation

A

Can easily be transferred through bacteria

Uptake of DNA from environment, DNA encodes gene that means that is resistant to antibiotic

108
Q

what happens in conjugation resistance transformation

A

Direct transfer of DNA between two microorganisms
Resistant bacteria conjugate with sensitive bacteria
When sensitive bacteria takes up plasmid copy now resistant

109
Q

what happens in transposons resistance transformation

A

Pieces of DNA that can jump
Will jump from chromosome become a piece of free DNA and then jump into new cell chromosome
Make sensitive strain resistant

110
Q

what happens in VRSA resistant mechanism

A

Three different enzymes that make D-Lac and D-Ala, enzymes also cleave off parallel D-Ala-D-Ala and replace with D-Ala-D-Lac
Results in peptide with D-Ala-D-Lac at end
Transpeptide can cleave D-Lac and get vancomycin resistance

111
Q

what are the three different enzymes that make D-LAc D-Ala

A

vanH
vanA
vanX

112
Q

what is VRSA resistant mechanism like

A

Involves many enzymes, encoded in big operon of genes

Operon has genes for regulation – sensing of vancomycin, turning on activator gene

113
Q

what are the four major types of antibiotics target in protein synthesis

A

1) Aminoglycosides
2) Tetracyclines
3) Macrolides
4) Chloramphenicol

114
Q

what do antibiotics targeting protein synthesis bind to

A

All bind to subunits of the ribosomes, but inhibit protein synthesis via different routes

115
Q

what do all aminoglycosides contain

A

can vary but they all contain a cyclohexane ring and amino sugars

116
Q

where are most aminoglycosides isolated from

A

Most are isolated from members of the bacterial genus Streptomyces

117
Q

what are aminoglycosides like

A

bactericidal (cause bacterial death)

118
Q

what do aminoglycosidaes binding killing mechanism

A

Bind to 30S small ribosome subunit, inhibiting protein synthesis or misreading of mRNA

119
Q

what is aminoglycosides msireading killing mechanism

A

Misreading of mRNA lead to modified proteins – if secreted can lead to activation of bacterial stress response – this can then lead to hydroxyl radicals formation

120
Q

is aminoglycosidase an effective antibiotic

A

two effects = effective bactericidal drug

121
Q

what are tetracyclines like

A

a group of antibiotics, all structurally similar consisting of a 4-ring structure with various attached side chains

122
Q

what are the two natural tetracyclines

A

Oxytetracycline and Chlortetracycline

123
Q

how are the two natural tetracyclines made

A

by the bacterial genus Streptomyces

124
Q

what are tetracyclines like

A

bacteriostatic – they stop cells replicating (they do not kill the bacteria)

125
Q

what do tetracyclines bind

A

Act by binding to the 30S subunit of ribosomes (similar to aminoglycosides)

126
Q

what are tetracyclines active against

A

Tetracyclines are active against most types of bacteria, including those that grow intracellularly within hosts

127
Q

what are the characteristics of tetracyclines

A

has 4 rings

128
Q

what do macrolides contain

A

contain a lactone ring – a ring structure of between 12 and 22 carbons

129
Q

what is the lactone ring in macrolides connected to

A

lactone ring is connected to one or more sugars

130
Q

what do macrolides bind to

A

Bind to the 50S ribosomal subunit (also called the 23S rRNA)

131
Q

what do macrolides inhibit

A

inhibit protein synthesis by stopping the elongation of the peptide chain

132
Q

what are macrolides like

A

bacteriostatic – they stop replication, but do not kill the bacteria

133
Q

what does chloramphenicol bind to

A

macrolides, binds to 50S subunit of ribosomes

134
Q

what is chloramphenicol like

A

bacteriostatic - inhibit bacterial growth

toxic

135
Q

what does chloramphenicol inhibit

A

protein synthesis

136
Q

what is chloramphenicol originally isolated from

A

Streptomyces venezualae

137
Q

what is chloramphenicol used for

A

toxic, so is only used for infections where there are no alternatives
used for eye infections as a topical antibiotic treatment

138
Q

what are the two major types of antibiotics target nucleic acid synthesis

A

1) Quinolones and Fluoroquinolones

2) Rifampicin

139
Q

what does quinolones target

A

target DNA replication

140
Q

what does rifampicin inhibit

A

Rifampicin inhibits RNA synthesis

141
Q

what are quinolones and rifampicin like

A

both types are bactericidal – resulting in bacterial cell death

142
Q

what are quinolones like

A

synthetic drugs

143
Q

what do quinolones contain

A

4-quinolone ring

144
Q

what does quinolones inhibit

A

the two topoisomerases: DNA gyrase and topoisomerase II

145
Q

what does DNA gyrase do

A

helps separate strands of DNA during replication and repair, without it both replication and repair of DNA cannot happen

146
Q

what do fluoroquinolones contain

A

a 4-quinolone ring

147
Q

what do Fluoroquinolones include

A

norfloxacin and ciprofloxacin

148
Q

what are norfloxacin and ciprofloxacin used for

A

regularly treat infections

149
Q

what do Fluoroquinolones

inhibit

A

inhibit topoisomerase II

150
Q

what do topoisomerases do

A

helps separate strands of DNA during replication and repair

151
Q

what are fluoroquinolones like

A

bactericidal – resulting in the death of bacterial cells

152
Q

what are rifamycin

A

Most are semisynthetic drugs

153
Q

what do rifamycins inhibit, effect

A

inhibiting RNA polymerase – stops the bacteria from transcribing genes – has a bactericidal result

154
Q

how does rifamycin have bacterial resistance

A

readily acquired by mutations in gene rpoB which encodes for RNA polymerase protein

155
Q

what is rifamycin used with

A

Often used in conjunction with other antibiotics to combat this easily acquired resistance

156
Q

what are the two major types of antibiotics target nucleic acid synthesis

A

1) Sulfonamides

2) Trimethoprim

157
Q

what do sulfonamides and trimethoprim inhibit

A

inhibit folic acid synthesis

158
Q

what is sulfonamides like

A

bacteriostatic

159
Q

what is trimethoprim like

A

bacteriostatic

160
Q

what are the other two antibiotics targeting metabolic processes with very narrow range of use

A

Dapsone

Isoiazid

161
Q

what are dapsone and isoiazid used for

A

less-well understood and are primarily used for mycobacterial infections such as leprosy or tuberculosis

162
Q

what are sulfonamides structurally related to

A

sulfanilamide

163
Q

what is an analogue of sulfanilamide

A

p-aminobenzoic acid

164
Q

what is p-aminobenzoic acid needed for

A

folic acid (folate) synthesis

165
Q

what do Sulfonamides compete with

A

p-aminobenzoic acid

166
Q

effect of Sulfonamides competing with p-aminobenzoic acid

A

reduction in the amount of folic acid synthesised

167
Q

what is folic acid

A

precursor of purines and pyrimidines

168
Q

what causes cessation of DNA

A

bases used for constructing DNA

results in cessation of DNA replication and protein synthesis

169
Q

what are sulfonamides like

A

bacteriostatic – they stop bacteria from replicating

170
Q

what is trimethoprim

A

synthetic antibiotic

171
Q

what does trimethoprim do

A

blocks folic acid synthesis by inhibiting enzyme tetrahydrofolate reductase

172
Q

what does trimethoprim compete with

A

dihydrofolic acid

173
Q

what does trimethoprim and dihydrofolic acid compete with

A

enzyme binding site, reducing folic acid production, so affecting DNA replication and protein synthesis

174
Q

what is Trimethoprim like

A

bacteriostatic antibiotic

175
Q

antimicrobial peptides examples

A

Polymyxin B and Colistin

176
Q

how do antimicrobial peptides act

A

they act by binding to, altering cell membrane structure of Gram-negative bacteria

177
Q

what does antimicrobial peptides bind to

A

binds to lipopolysaccharide (LPS) and alter bacterial outer membrane permeability

178
Q

what happens in the cytoplasmic membrane

A

fatty acid portion of polymyxin dissolves and disrupts membrane integrity

179
Q

do antimicrobial peptides have side effects

A

have significant side effects

including neurotoxicity and renal necrosis deemed a ‘last-resort’ antibiotic

180
Q

what is colistin referred as

A

last-resort for multi-drug resistant Klebsiella

181
Q

where does colistin bind to

A

LPS in outer membrane of Gram-negative bacteria

182
Q

what causes colistin resistance

A

due to a change in lipid A structure moiety

single base pair mutation in genes for regulators of lipid A modifying enzymes

183
Q

how does lipid A structure vary

A

lipid A structure varies between species and a variety of different modifications can be made to structure within cell including addition of extra fatty acids

184
Q

what are streptomyces a source of

A

many natural antibiotics

185
Q

where are streptomyces found

A

soil

186
Q

why does soil smell

A

streptomyces gives soil its characteristic smell

187
Q

what new antibiotic may have hope

A

teixobactin

188
Q

where are antibiotics in the environment

A

Wastewater treatment plants – levels of total nitrogen measured in effluent NOT levels of bacteria

189
Q

example of antibiotics used in plant treatment

A

fire blight on apples and pears, treated with streptomycin and tetracycline

190
Q

example of antibiotics used in veterinary

A

Therapeutic and prophylactic treatment of animals

191
Q

examples of antibiotic use in animal feed as growth promoter

A

Used at subtherapeutic levels
WHO recognises it as a global problem
Shouldn’t be antibiotics used in human therapeutics
BUT structural relatedness of drugs means resistance to one drug can cause cross-resistance to others

192
Q

where can antibiotic residues be found in food chain

A

Present if cow being treated for mastitis (udder infection)

193
Q

what does fermentation of yoghurt and cheese production require

A

Fermentations requiring addition of live bacteria (starter cultures) to produce flavours and textures associated with these products

194
Q

effect of antibiotics on yoghurt and cheese production

A

Antibiotics present in milk kill starter culture or reduce activity resulting in poor or no fermentation and hence poor quality product or product failure

195
Q

how has cross resistance developed

A

Apramycin resistance is due to acquisition of an aminoglycoside acetyltransferase 3-IV (aac(3)-IV)
apramycin resistance confers resistance to gentamicin

196
Q

what is apramycin used for

A

an antimicrobial used to treat serious infections in hospitals

197
Q

is apramycin used to treat humans

A

never being used to treat humans, resistant strains of E. coli, Salmonella & Klebsiella pneumoniae in humans emerged

198
Q

what are the antibiotic levels like in natural antibodies

A

very low

199
Q

what makes nisin

A

Lactococcus lactis

200
Q

what does nisin inhibit

A

inhibit a range of Gram-positive bacteria

201
Q

what is nisin used for

A

stop gram-positive bacteria e.g. Clostridium, Bacillus, Staphylococcus in canned foods, dairy products, chocolate, sauces

202
Q

what is natamycin

A

antifungal

203
Q

what is antifungal used for

A

used on surface of sausages and cheeses and peanuts

204
Q

what are the ESKAPE pathogens

A 
Enterococcus faecium
Staphylococcus aureus
Klebsiella pneumoniae
Acinetobacter baumannii
Pseudomonas aeruginosa
Enterobacter
205
Q

what do ESKAPE cause

A

Majority of infections in nosocomial environment

Microbes and You (14 decks)

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