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lecture 8) antibiotics 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
how do fluoroquinolines get into gram positive and gram negative bacteria?
passively diffuse into gram positives | via outer membrane porins in gram negatives
26
what are the newer fluoroquinolines like?
broader spectrum | better activity against gram positives
27
describe cephalosporins
broad spectrum semi synthetic Beta lactam
28
where do cephalosporins come from?
derived from mould cephalosporins
29
what are cephalosporins chemically related to?
penicillins
30
what type of cells do penicillins work on?
actively dividing cells
31
what is the mode of action of penicilins?
in cell wall synthesis carbohydrate linkages break | penicillins prevent the peptide bonds from linking
32
what is the consequence of penicillins mode of action?
preventing the linkage of the peptide bonds means the cell wall will be weaker bacterial cells will die due to osmotic shock
33
describe the mode of action of beta lactam antibiotics
interfere with cell wall synthesis
34
what type of antibiotics are beta lactams?
bactiolytic
35
what are carbapenamases?
aggressive beta lactams
36
what type of bacteria are resistant to carbapenamase? how are they resistant?
enterobacteria eg e coli | enzymatic breakdown of carbapenamase
37
what is the risk of using one antibiotic a lot?
lots of use = more likelihood of resistance
38
what do novel antibiotics aim to target and why?
broad range of targets in bacterial pathogens so they can be used for more than one condition
39
why would it be a bad idea to target essential cellular processes?
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
name the 5 stages of infection
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
describe the process of adsorption to receptor in the first stage of infection
phage attachment is specific
42
describe the two types of receptors for adsorption in the first stage of infection
``` surface components (some bacteria have generated enzymes that degrade the EPS therefore covering the receptor) sex pillus for male specific F+ phages ```
43
how does the lytic phage inject its DNA into the host?
after degrading peptidoglycan and forming pores in the cell wall, lytic DNA is transferred into cell phage DNA hijacks hosts machinery
44
what is responsible for bacterial cell lysis and phage progeny release?
phage protein inhibitors responsible for host cell lysis and virion burst to environment
45
give some examples of phage protein inhibitors
lysins holins mureins
46
name a technique used to analyse bacteriophages killing cells
plaque assays
47
what is the difference between lysis and lysogeny?
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
how are lysis and lysongey interchanged?
genetic switch
49
give 2 advantages of lytic phages
specific | cheap
50
give 2 disadvantages of lytic phages
narrow spetrum | bacterial resistance
51
describe what would be the case when using individual phages
narrow spectrum higher pretreatment costs (pretesting and phage bank) 1 phage isnt as good of a antimicrobial
52
describe a less complex cocktail of phages
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
describe more complex cocktails
greater ease of use potentially greater complexity in manufacture and outcomes more broad spectrum
54
describe typical commercial antibiotics
they have a greater impact on normal microbiota | more unknown physiologies during their development
55
describe the balance needed in antibiotics
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
what is the collateral damage if antibiotics?
dysbiosis ie disturbing the gut microbiome
57
describe an alternative phage strategy
use the phage to deliver a protein that interferes with an essential process rendering the bacteria more susceptible to antibiotics
58
what is the SOS response?
a programme elicited from bacteria in response to detection of DNA damage
59
how could you inhibit the SOS response to make the bacteria more susceptible to antibiotics?
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
what is the CRISPR associated system (Cas)?
a defence strategy employed by bacteria
61
what can be targetted when phage deliver Cas to the bacteria?
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
what is the baseline level of expression of toxin antitoxin systems?
degradation of the toxin mediated by going into growth arrest
63
give a general overview of antivirulence strategies
inhibit specific mechanisms that promote infection and that are essential to persistence
64
what would antivirulence strategies offer in terms of mutations?
reduced selection pressure for drug-resistant mutations
65
what would virulence specific therapeutics avoid?
dysbiosis as they are more specific treatments that antibiotics preventing disturbance to the gut microbiota
66
what is the most common cause of HCAIs and UTIs?
UPEC (uropathogenic escherichia coli)
67
how does UPEC invade the host?
invades with pili on the surface that facilitates interaction with host
68
what are IBCs?
intracellular bacterial communities
69
how do IBCs cause infection?
replicate, burst, spread
70
what type of cells are included in IBCs?
facet cells
71
in what manner do type I and II pilli binds to europlakin on facet cells?
carbohydrte dependent manner | lectin binding domain
72
what is a pilicide?
agent that removes pili on UPEC deeming it unable to cause infection
73
why is quorum sensing important for virulence?
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
what is used in the identification of inhibitors?
reporter strains
75
name the autoinducer in QS of gram positive bacteria
AIP (autoinducing peptide)
76
name the signalling molecule in QS of gram negative bacteria
AHL (N- aceyl homoserine lactones)
77
how would you prevent QS in gram positive bacteria?
inhibit the production of AIP deeming it unable to cause infection
78
how would you prevent QS in gram negative bacteria?
block the AHL receptor making it unable to cause infection
79
why might QS not be direct enough?
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
why type of toxin does cholera release?
AB toxin (exotoxin)
81
what is the name of the protein that causes the toxic effects of cholera?
ToxT
82
what is virstatin?
a small molecule that inhibits ToxT transcription therefore preventing infection
83
what is responsible for the expression of ToxT?
transcription factor in V. cholerae
84
what is the possible collateral damage when inhibiting the ToxT gene in V. cholerae?
the transcription factor could encode for other genes
85
what is an alternative to targetting the transcription factor of ToxT in V. cholerae?
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
what was discovered to inhibit secretion systems that didnt lack potency and a clear mode of action?
ATPase YscN which is essential for T3SS in Y. pestis
87
what secretion systems in gram negative bacteria inject effect molecules into host cell and cause disease?
type 3 and 4
88
give an example of 2 bacteria that use type 3/4 secretion systems to inject their effector molecules into the host cell
salmonella and heliobacter pylori
89
what are T3SS related to?
flagella (how bacteria move)
90
what are T4SS related to?
conjugation pillus (how bacteria mate)
91
how would you inhibit the activity of T3 and 4SS in flagella and conjugation pillus?
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
what is a synergistic drug?
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
what is the impact of synergistic drugs on subpopulations?
suppresses drug resistant subpopulations more than a single drug therapies
94
what is the consequence of suppressing drug resistant subpopulations?
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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