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microbiology > lecture 8) antibiotics > Flashcards

lecture 8) antibiotics Flashcards

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Biology 101 flashcards
1
Q

describe bacteriostatic modes of action

A

total and viable cell count plateau out on addition of antibiotic
doesnt kill any cells

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2
Q

describe bacteriocidal mode of action

A

kills viable cells

total cells plateau on addition of antibiotics; cells are still there but they are unable to divide as they are dead

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3
Q

describe bacteriolytic mode of action

A

total and viable cell counts completely deplete as dead cells diasppear

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4
Q

give an example of a bacteriostatic antibiotic

A

fluoroquinolines

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5
Q

why are fluoroquinolines an example of bacteriostatic antibiotic?

A

they inhibit protein synthesis

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6
Q

why can fluoroquinolines be considered a bacteriocidal antibiotic too?

A

they can damage DNA

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7
Q

why is there a motivation to discover more essential cell processes?

A

antibiotics normally target essential cellular processes therefore by finding more essential cell processes they could be potential targets for new antibiotics to combat the issue of antibiotic resistance

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8
Q

what do bacteriostatic antibiotics target?

A

cellular processes eg protein synthesis

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9
Q

what do bacteriolytic antibiotics target?

A

cell synthesis eg ABs that cause lysis forming pores in cell membrane/wall

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10
Q

what are macrolides?

A

they are a class of antibiotic

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11
Q

what is the binding site of a macrolide on a bacterial cell?

A

a large ribosomal subunit in the upper part of the nascent peptide

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12
Q

what is the large ribosomal subunit in the upper nascent peptide responsible for?

A

it is an exit tunnel for proteins to pass through

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13
Q

what is the mode of action of a macrolide?

A

binds to the large ribosomal subunit in the upper part of the nascent peptide, blocking the exit tunnel for proteins therefore proteins wont be able to leave the ribosome therefore translation is inhibited
growth arrest

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14
Q

what is the primary target of fluoroquinolines?

A

DNA gyrase

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15
Q

what is another name for DNA gyrase?

A

topoisomerase II

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16
Q

what is the function of DNA gyrase?

A

involved in the binding of DNA

also fragments DNA which isnt ideal

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17
Q

what is the secondary target of fluoroquinolines?

A

topiosomerase IV

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18
Q

describe the structure of topiosomerase II

A

heterotetramer

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19
Q

name the subunits in topiosomerase II

A

2 ParC subunits

2 ParE subunits

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20
Q

the protein that encodes for ParC subunits is homologous to what subunit of DNA gyrase?

A

subunit A

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21
Q

the protein that encodes for ParE subunits is homologous to what subunit in DNA gyrase?

A

subunit B

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22
Q

what is topiosomerase responsible for in DNA?

A

the decantation and relaxation of DNA

assists with segregation of replicating chromosomes/plasmids in bacteria

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23
Q

if topiosomerase was inhibited, what would be the outcome in bacteria?

A

decantation and relaxation of DNA and segregation of replication chromosomes/plasmids would be inhibited

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24
Q

describe the fluoroquinoline mode of action on bacteria

A

they inhibit DNA gyrase aka topiosomerase II that is involved in the relaxation and decantation of DNA and the segregation of chromosomes and plasmids
these processes wont happen if DNA gyrase is inhibited

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25
Q

how do fluoroquinolines get into gram positive and gram negative bacteria?

A

passively diffuse into gram positives

via outer membrane porins in gram negatives

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26
Q

what are the newer fluoroquinolines like?

A

broader spectrum

better activity against gram positives

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27
Q

describe cephalosporins

A

broad spectrum
semi synthetic
Beta lactam

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28
Q

where do cephalosporins come from?

A

derived from mould cephalosporins

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29
Q

what are cephalosporins chemically related to?

A

penicillins

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30
Q

what type of cells do penicillins work on?

A

actively dividing cells

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31
Q

what is the mode of action of penicilins?

A

in cell wall synthesis carbohydrate linkages break

penicillins prevent the peptide bonds from linking

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32
Q

what is the consequence of penicillins mode of action?

A

preventing the linkage of the peptide bonds means the cell wall will be weaker
bacterial cells will die due to osmotic shock

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33
Q

describe the mode of action of beta lactam antibiotics

A

interfere with cell wall synthesis

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34
Q

what type of antibiotics are beta lactams?

A

bactiolytic

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35
Q

what are carbapenamases?

A

aggressive beta lactams

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36
Q

what type of bacteria are resistant to carbapenamase? how are they resistant?

A

enterobacteria eg e coli

enzymatic breakdown of carbapenamase

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37
Q

what is the risk of using one antibiotic a lot?

A

lots of use = more likelihood of resistance

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38
Q

what do novel antibiotics aim to target and why?

A

broad range of targets in bacterial pathogens so they can be used for more than one condition

39
Q

why would it be a bad idea to target essential cellular processes?

A

we know that bacteria will develop a resistance mechanism for these bacteria as they want to live so will find a way to prevent this antibiotic from attacking them

40
Q

name the 5 stages of infection

A

adsorption to specific receptor
DNA injection
redirection of host metabolism to phage DNA replication and phage DNA protein synthesis
assembly and packaging of phage particles
bacterial cell lysis and phage progeny release

41
Q

describe the process of adsorption to receptor in the first stage of infection

A

phage attachment is specific

42
Q

describe the two types of receptors for adsorption in the first stage of infection

A 
surface components (some bacteria have generated enzymes that degrade the EPS therefore covering the receptor)
sex pillus for male specific F+ phages
43
Q

how does the lytic phage inject its DNA into the host?

A

after degrading peptidoglycan and forming pores in the cell wall, lytic DNA is transferred into cell
phage DNA hijacks hosts machinery

44
Q

what is responsible for bacterial cell lysis and phage progeny release?

A

phage protein inhibitors responsible for host cell lysis and virion burst to environment

45
Q

give some examples of phage protein inhibitors

A

lysins
holins
mureins

46
Q

name a technique used to analyse bacteriophages killing cells

A

plaque assays

47
Q

what is the difference between lysis and lysogeny?

A

lysogeny is the integration of the bacteriophage nucleic acid into the host’s bacterial genome
lysis is the packaging and release of the phage

48
Q

how are lysis and lysongey interchanged?

A

genetic switch

49
Q

give 2 advantages of lytic phages

A

specific

cheap

50
Q

give 2 disadvantages of lytic phages

A

narrow spetrum

bacterial resistance

51
Q

describe what would be the case when using individual phages

A

narrow spectrum
higher pretreatment costs (pretesting and phage bank)
1 phage isnt as good of a antimicrobial

52
Q

describe a less complex cocktail of phages

A

potential requirement for development of a diverse range of individual cocktails (cocktail bank)
not as narrow spectrum
to decrease resistance a diverse range needs to b developed

53
Q

describe more complex cocktails

A

greater ease of use
potentially greater complexity in manufacture and outcomes
more broad spectrum

54
Q

describe typical commercial antibiotics

A

they have a greater impact on normal microbiota

more unknown physiologies during their development

55
Q

describe the balance needed in antibiotics

A

need it to be not too low so as its too narrow spectrum and therefore not killing enough of the bacterial strains and it being too broad and therefore killing some of the natural microbiota

56
Q

what is the collateral damage if antibiotics?

A

dysbiosis ie disturbing the gut microbiome

57
Q

describe an alternative phage strategy

A

use the phage to deliver a protein that interferes with an essential process rendering the bacteria more susceptible to antibiotics

58
Q

what is the SOS response?

A

a programme elicited from bacteria in response to detection of DNA damage

59
Q

how could you inhibit the SOS response to make the bacteria more susceptible to antibiotics?

A

engineer bacteriophage to inject DNA into host cell
engineer a protein called Xa3 which will be turned on during SOS response
Xa3 will inhibted SOS response making bacteria more susceptible to antibiotics

60
Q

what is the CRISPR associated system (Cas)?

A

a defence strategy employed by bacteria

61
Q

what can be targetted when phage deliver Cas to the bacteria?

A

essential proteins on plasmid/DNA
toxin antitoxin system which would prevent persister cell formation
phage could also be used to mediate effects on bacteria

62
Q

what is the baseline level of expression of toxin antitoxin systems?

A

degradation of the toxin mediated by going into growth arrest

63
Q

give a general overview of antivirulence strategies

A

inhibit specific mechanisms that promote infection and that are essential to persistence

64
Q

what would antivirulence strategies offer in terms of mutations?

A

reduced selection pressure for drug-resistant mutations

65
Q

what would virulence specific therapeutics avoid?

A

dysbiosis as they are more specific treatments that antibiotics preventing disturbance to the gut microbiota

66
Q

what is the most common cause of HCAIs and UTIs?

A

UPEC (uropathogenic escherichia coli)

67
Q

how does UPEC invade the host?

A

invades with pili on the surface that facilitates interaction with host

68
Q

what are IBCs?

A

intracellular bacterial communities

69
Q

how do IBCs cause infection?

A

replicate, burst, spread

70
Q

what type of cells are included in IBCs?

A

facet cells

71
Q

in what manner do type I and II pilli binds to europlakin on facet cells?

A

carbohydrte dependent manner

lectin binding domain

72
Q

what is a pilicide?

A

agent that removes pili on UPEC deeming it unable to cause infection

73
Q

why is quorum sensing important for virulence?

A

signal communication between cells to activate the transcription of genes to code for more virulent cells
one cell wont cause an infection but multiple will therefore QS makes more virulent cells to cause disease

74
Q

what is used in the identification of inhibitors?

A

reporter strains

75
Q

name the autoinducer in QS of gram positive bacteria

A

AIP (autoinducing peptide)

76
Q

name the signalling molecule in QS of gram negative bacteria

A

AHL (N- aceyl homoserine lactones)

77
Q

how would you prevent QS in gram positive bacteria?

A

inhibit the production of AIP deeming it unable to cause infection

78
Q

how would you prevent QS in gram negative bacteria?

A

block the AHL receptor making it unable to cause infection

79
Q

why might QS not be direct enough?

A

in order to prevent infection the pathogen and its communities must be alive not just the AV factor as there can be cross talk between the cells

80
Q

why type of toxin does cholera release?

A

AB toxin (exotoxin)

81
Q

what is the name of the protein that causes the toxic effects of cholera?

A

ToxT

82
Q

what is virstatin?

A

a small molecule that inhibits ToxT transcription therefore preventing infection

83
Q

what is responsible for the expression of ToxT?

A

transcription factor in V. cholerae

84
Q

what is the possible collateral damage when inhibiting the ToxT gene in V. cholerae?

A

the transcription factor could encode for other genes

85
Q

what is an alternative to targetting the transcription factor of ToxT in V. cholerae?

A

receptor mimics - make something that looks like the receptor but has a higher affinity for the toxin than the actual receptor so the toxin binds to it preventing infection

86
Q

what was discovered to inhibit secretion systems that didnt lack potency and a clear mode of action?

A

ATPase YscN which is essential for T3SS in Y. pestis

87
Q

what secretion systems in gram negative bacteria inject effect molecules into host cell and cause disease?

A

type 3 and 4

88
Q

give an example of 2 bacteria that use type 3/4 secretion systems to inject their effector molecules into the host cell

A

salmonella and heliobacter pylori

89
Q

what are T3SS related to?

A

flagella (how bacteria move)

90
Q

what are T4SS related to?

A

conjugation pillus (how bacteria mate)

91
Q

how would you inhibit the activity of T3 and 4SS in flagella and conjugation pillus?

A

ATP dependent processes therefore if you prevent the ATPase no ATP will be produced so the secretion systems wont be able to work and wont be able to cause infection
this is tricky because the ATPase may be generating ATP for other processes

92
Q

what is a synergistic drug?

A

when 2 or more drugs are used and they work together to produce a response that would be more potent if they were used in isolation

93
Q

what is the impact of synergistic drugs on subpopulations?

A

suppresses drug resistant subpopulations more than a single drug therapies

94
Q

what is the consequence of suppressing drug resistant subpopulations?

A

eliminates competitors of the drug resistant strains so they will grow more rapidly therefore increasing the population density

microbiology (17 decks)

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