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GERR > Lecture 44: Antibacterials > Flashcards

Lecture 44: Antibacterials Flashcards

1
Q

what are the 2 most important classes of antibiotics that act on the bacterial cell wall

A
  • beta lactams

- glycopeptides

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2
Q

what was the first beta lactic discovered

A

penicillin

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3
Q

what are the 4 main classes of beta lactams

A
  • penicillins
  • cephalosporins
  • carbapenems
  • monobactams
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4
Q

what is penicillin betalactamase inhibitor combinations (BLICs)

A

a beta lactam combined w/ molecule designed to make antibiotic less susceptible to breakdown

  • bacteria less likely to be resistant to BLICs than to penicillins
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5
Q

describe beta lactam antibacterial MoA

A
  • bacterial cell wall composed of peptidoglycan
  • peptidoglycan chains cross linked by transpeptidase enzyme
  • -> aka penicillin binding protein
  • PBPs inhibited by beta lactams
  • cell wall severely weakened
  • results in bacterial cell lysis
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6
Q

what is present in the structure of all beta lactams

A

beta lactam ring

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7
Q

what is the difference in peptidoglycan between gram +ve and gram -ve bacteria

A

thickness differs

  • thicker in gram +ve
  • thinner in gram -ve
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8
Q

what type of bacteria does benzylpenicillin mainly act on

A

gram +ve bacteria

  • specifically beta-haemolytic streptococci
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9
Q

how is penicillin usually administered

A

IV (benzylpenicillin)

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10
Q

give examples of oral penicillin

A
  • phenoxymethylpenicillin

- penicillin V

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11
Q

why are oral penicillins not usually used

A

they are poorly absorbed

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12
Q

what are oral penicillins normally used to treat

A

streptococcal tonsilitis

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13
Q

what is the main pathogen target of benzylpenicillin and oral penicillins

A

beta-haemolytic streptococci

- group A strep

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14
Q

what is benyzlpenicillin typically used to treat

A
  • streptococcal tonsillitis

- streptococcal cellulitis/ soft tissue infection

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15
Q

what penicillin drug has better oral absorption than penicillin V

A

amoxicillin

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16
Q

what is amoxicillin used for

A

used as step-down from benzylpenicillin, acts against:

  • strep pneumoniae
  • beta-haemolytic streptococci
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17
Q

what is amoxicillin a treatment choice for

A
  • pneumonia

- infections caused by enterococcus faecalis and listeria monocytogenes

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18
Q

what are the main pathogen targets of amoxicillin

A
  • strep pneumoniae
  • listeria monocytogenes
  • enterococcus faecalis
  • beta-haemolytic streptococci
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19
Q

what are the common clinical indications of amoxicillin

A
  • chest infection
  • community acquired pneumonia
  • listeria infections
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20
Q

how is amoxicillin prepared

A

IV and oral

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21
Q

why might amoxicillin not be sufficient by itself as treatment for enterococci

A

enterococci frequently part of polymicrobial infection

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22
Q

what is flucloxacillin the treatment choice for

A

staphyloccocal aureus infection

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23
Q

what is the main pathogen target of flucloxacillin

A

staph aureus

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24
Q

what are the clinical indications of flucloxacillin

A
  • skin/soft tissue infection
  • bone/joint infection
  • endocarditis
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25
Q

how is flucloxacillin prepared

A

IV and PO

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26
Q

what type of class betalactam is aztreonam

A

monolactam

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27
Q

what organisms is aztreonam activity limited to

A

gram -ve organisms

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28
Q

what are the clinical indications of aztreonam

A
  • UTI
  • as part of combination therapy for:
  • -> intra-abdominal infections
  • -> hospital acquired chest infections
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29
Q

how is aztreonam prepared

A

IV

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30
Q

when might aztreonam be used

A

in combination w/ other antibiotics in Px w/ penicillin allergy

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31
Q

what class of beta lactam are ceftriaxone and cefotaxime

A

third generation cephalosporins

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32
Q

what are 3 important things to remember regarding ceftriaxone and cefotaxime

A
  • ceftriaxone is recognised cover for syphilis while cefotaxime is not
  • ceftriaxone is contraindicated in neonates b/c it can displace bilirubin from binding to albumin –> hyperbilirubinaemia and potentially bilirubin encephalopathy
  • ceftriaxone is drug on formulary for adults in most hospitals
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33
Q

what are the main pathogen targets of ceftriaxone and cefotaxime

A
  • neisseria meningitidis
  • streptococcus pneumoniae
  • staph aureus
  • beta-haemolytic streptococci
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34
Q

what are the clinical indications for ceftriaxone and cefotaxime

A
  • meningitis
  • OPAT (out px parenteral antimicrobial therapy)
  • soft tissue infection
  • intra-abdominal infections
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35
Q

how are ceftriaxone and cefotaxime prepared

A

IV

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36
Q

what is the second most important class of antibiotics that act on bacterial cell wall

A

glycopeptides

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37
Q

give the two main antibiotics in glycopeptide class

A
  • vancomycin

- teicoplanin

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38
Q

what are the only type of bacteria that glycopeptides are active against and why

A
  • gram +ve bacteria

- large polar molecules that are too bulky to penetrate the external membrane of gram -ve bacteria

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39
Q

why do glycopeptides stay in the anatomical compartment they are administered in

A

they are so big that they don’t easily cross membranes

if given orally –> stay in gut
if given IV –> stay in blood

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40
Q

describe the MoA of Glycopeptides and how they differ to beta lactams

A
  • Glycopeptides bind to peptidoglycan preventing peptidoglycan formation
  • glycopeptides inhibit cell wall synthesis earlier than beta lactams; beta lactams act at a later stage inhibiting the cross linking of peptidoglycans
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41
Q

what is the key pathogen that glycopeptides act against

A

staph aureus esp MRSA

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42
Q

what are the main pathogen targets of Teicoplanin

A
  • MRSA

- gram +ves

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43
Q

what are the clinical indications of Teicoplanin

A
  • OPAT (out px parenteral antimicrobial therapy)
  • -> soft tissue infection
  • -> intra abdominal allergies
  • combination therapy in penicillin allergy
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44
Q

how is Teicoplanin prepared

A

IV only

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45
Q

how does the use of Teicoplanin and vancomycin differ

A
  • spectrum of activity basically identical
  • Teicoplanin can be give OD so more freq. used in OPAT
  • vancomycin can be taken PO for C diff
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46
Q

what are the main pathogen targets for vancomycin

A
  • MRSA
  • C diff
  • gram +ves
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47
Q

what are the clinical indications of vancomycin

A
  • soft tissue infection
  • combination therapy in penicillin allergy
  • C diff colitis (only indication for PO)
  • intra abdominal infections
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48
Q

how is vancomycin prepared

A
  • PO only for C diff

- IV only for all other infections

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49
Q

what are the 3 categories of antibiotics that act within the cell (non cell-wall active agents)

A
  • protein synthesis inhibitors
  • nucleic acid synthesis inhibitors
  • miscellaneous antibiotics
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50
Q

what are the 3 classes of protein synthesis inhibitors

A
  • macrolides
  • aminoglycosides
  • tetracyclines
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51
Q

what are the 3 most common macrolides and when is each most commonly prescribed

A
  • clarithromycin –> predominantly prescribed
  • erythromycin –> macrolide of choice in pregnancy
  • azithromycin –> used by chest physicians
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52
Q

why is clarithromycin more predominantly prescribed

A
  • it is better tolerated (erythromycin ^ gut motility and can cause nausea/vomiting/diarrhoea
  • has better bioavailability (50-55% for clarithromycin vs 15-45% for erythromycin)
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53
Q

what is bioavailability

A

fraction of the administered drug that reaches the systemic circulation (always 100% for IV drugs by definition)

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54
Q

what are atypical bacteria, give examples, and what do they cause

A
  • bacteria w/ cell wall deficit
  • legionella
  • chlamydia
  • mycoplasma
  • cause atypical pneumonias
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55
Q

what pathogens do macrolides have the most important activity against

A

cell wall deficit atypical bacteria

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56
Q

what are the main pathogen targets of clarithromycin

A
  • strep pneumoniae
  • haemophilus influenzae
  • atypical chest pathogens
  • -> legionella pneumophila
  • -> chlamydia trachomatis
  • -> mycoplasma pneumoniae
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57
Q

what is the clinical indication of clarithromycin

A

chest infections

58
Q

how can clarithromycin be prepared

A

IV or oral

59
Q

how is clarithromycin primarily used in hospital setting for CAP

A

in combination w/ beta lactam

60
Q

what are the 3 most common aminoglycosides and when are they most commonly used

A
  • gentamicin - 1st line
  • amikacin - slightly better against highly resistant gram -ves
  • tobramycin - slightly better pseudomonas cover
61
Q

what pathogen is inherently resistant to aminoglycosides and how is this over come

A
  • streptococci
  • use aminoglycosides in combination of beta lactam which breaks down cell wall to allow amino glycoside access to bacterial ribosome
62
Q

what are the main pathogen targets for aminoglycosides

A
  • staphylococci

- gram -ves

63
Q

what are the clinical indications of aminoglycosides

A
  • sepsis

- UTI

64
Q

how are aminoglycosides prepared

A

IV only

65
Q

what are the most important clinical features of aminoglycosides

A
  • rapidly bactericidal

- synergistic effect w/ beta lactams

66
Q

what are the draw backs of aminoglycosides

A
  • nephrotoxicity and ototoxicity

- they’re hydrophilic so stay in ‘water ways’ i.e. ^ conc in blood and urine, don’t penetrate well into tissue

67
Q

what are the 3 most common tetracyclines

A
  • doxycycline
  • minocycline
  • tetracycline
68
Q

which tetracycline is most commonly used in hospital setting

A

doxycycline

69
Q

what are important contraindications of tetracyclines and why

A
  • children under 12
  • pregnancy
  • bind to calcium and deposited in actively calcifying teeth (results in staining) and bones of unborn/growing children
70
Q

what are the pathogen targets for doxycycline

A
  • MRSA isolates
  • staphylococci
  • streptococci
  • haemophilus influenzae
  • atypical chest pathogens
  • -> legionella pneumophila
  • -> chlamydia trachomatis
  • -> mycoplasma pneumoniae
71
Q

what are the clinical indications for doxycycline

A
  • chest infection

- oral MRSA treatment

72
Q

how is doxycline prepared

A

oral

73
Q

what are the 3 main classes of nucleic acid synthesis inhibitors

A
  • quinolones
  • nitroimidazoles (most common is metronidazole)
  • trimethoprim
74
Q

what are the 3 most common quinolones

A
  • ciprofloxacin (better in gram -ve)
  • levofloxacin
  • moxifloxacin (better in gram +ve)
75
Q

what is the MHRA health warning regarding the use of quinolones

A

should no longer be prescribed for non severe infections due to risk of tendonopathy and tendon rupture

76
Q

what are the main pathogen targets for ciprofloxacin

A
  • pseudonyms aeruginosa

- gram -ves

77
Q

what are the clinical indications of ciprofloxacin

A
  • oral treatment for pseudonyms aeruginosa

- part of combination therapy in penicillin allergic patients

78
Q

how is ciprofloxacin prepared

A

IV or oral

79
Q

why else is the use of ciprofloxacin restricted

A

assc. w/ MRSA and C diff

80
Q

what are the main pathogen targets of levofloxacin/moxifloxacin

A
  • streptococcus pneumoniae
  • atypical chest pathogens
  • haemophilus influenzae
81
Q

what are the clinical indications of levofloxacin/moxifloxacin

A

chest infection (CAP in penicillin allergic px

82
Q

how is levofloxacin/moxifloxacin prepared

A

IV or oral

83
Q

what is the only type of pathogen that metronidazole is active against

A

true anaerobes

84
Q

what are the main pathogen targets of metronidazole

A
  • anaerobes

- C diff

85
Q

what are the clinical indications of metronidazole

A
  • polymicrobial infections
  • -> intra abdominal infections
  • C diff colitis
86
Q

how is metronidazole prepared

A

IV or oral

87
Q

what is trimethoprim solely used for

A

treatment of uncomplicated lower UTIs

88
Q

what are the main pathogen targets of trimethoprim

A
  • aerobic gram -ves
  • -> E. coli
  • -> klebsiella
  • -> proteus
89
Q

what is the clinical indication of trimethoprim

A

uncomplicated lower UTIs

90
Q

how is trimethoprim prepared

A

oral

91
Q

what are the two examples of miscellaneous antimicrobials

A
  • nitrofurantoin

- fidaxomicin

92
Q

what are the main pathogen targets of nitrofurantoin

A
  • gram -ves

- enterococcus faecalis

93
Q

what is the only clinical indication of nitrofurantoin

A

uncomplicated lower UTIs

94
Q

how is nitrofurantoin prepared

A

oral only

95
Q

what are the contraindications of nitrofurantoin

A
  • px w/ glucose 6-phosphate dehydrogenase deficiency (risk of haemolytic anaemia)
  • at term in pregnancy (risk of Haemolysis of immature neonatal RBC)
  • px w/ renal impairment (reduced renal excretion –> treatment failure)
96
Q

what class of antibiotics is fidaxomicin the first of

A

macrocyclic

97
Q

what is the only indication of fidaxomicin

A

C diff colitis

98
Q

how is fidaxomicin prepared

A

oral only

99
Q

compare fidaxomicin and vancomycin in C diff treatment

A
  • fidaxomicin is as efficacious as oral vancomycin
  • fidaxomicin has lower risk of relapse
  • fidaxomicin is more expensive
100
Q

describe the 3 main types of resistance mechanisms that bacteria can have

A
  • enzymatic degradation
  • -> prod of enzymes that breakdown antibiotics
  • target site modification
  • -> alters site where antibiotic acts reducing efficacy
  • restricted access
  • -> efflux pumps actively remove antibiotic
  • -> membrane penetration barrier (down regulation in number of porins that give antibiotic access to bacterium - reduced permeability)
101
Q

what is the most important example of enzymatic degradation

A

resistance to beta lactams

  • -> beta lactamases (prod by both gram +ves and -ves
  • -> break down beta lactam ring
102
Q

which bacteria produce the most clinically important beta lactamases

A

gram -ves e.g. E.coli and klebsiella

103
Q

describe how antibiotics have been developed w/ more resilience to beta lactamases

A
  • inherent resilience
  • protector molecule added
  • -> penicillin-BetaLactamase Inhibitor Compounds (BLICs)
104
Q

what are the 2 most commonly encountered beta lactamase inhibitors

A
  • clavulanate –> combined w/ amoxicillin to form co-amoxiclav
  • tazobactam –> combined w/ piperacillin to form piperacillin-tazobactam
105
Q

outline how BLICs provide resilience to beta lactams

A
  • BLICs resemble beta lactam structure
  • protect antibiotic by:
  • -> acting as surrogate substrate for beta lactamase
  • -> binding to beta lactamase, permanently inactivating it
106
Q

describe the relationship between activity spectrum of beta lactams and their resilience to beta lactamases

A

the higher the spectrum of gram -ve activity, the lower the resilience to gram -ve beta lactamases

107
Q

what are the main pathogen targets of co-amoxiclav

A
  • gram -ves

- can be used broadly when pathogen unknown or likely polymicrobial infection

108
Q

what are the clinical indications of co-amoxiclav

A
  • intra abdominal (polymicrobial)
  • complicated UTIs (gram -ves)
  • complicated ENT infections
109
Q

how is co-amoxiclav prepared

A

IV or oral

110
Q

what are the main pathogen targets of piperacillin-tazobactam

A
  • pseudomonas aeruginosa

- gram -ves

111
Q

what are the clinical indications of piperacillin-tazobactam

A
  • sepsis

- infection in severely immunosuppressed px where source is unknown

112
Q

how is piperacillin-tazobactam prepared

A

IV

113
Q

which BLIC is better against gram -ves

A

piperacillin-tazobactam

114
Q

what is one of the broadest spectrum antimicrobials

A

meropenem

115
Q

what are the main pathogen targets of meropenem

A

almost anything

- breadth of cover is the most important aspect

116
Q

what are the clinical indications of meropenem

A
  • severe sepsis

- infection in severely immunosuppressed px where source is unknown

117
Q

how is meropenem prepared

A

IV

118
Q

what is the most clinically important beta-lactamase and why

A

carbapenemases

  • prod by gram -ves
  • capable of breaking down all beta lactams
  • usually no beta-lactam treatment options
  • gene encoding enzyme is plasmid mediated so can be passed between bacteria of the same or different genera
119
Q

what does carbapenemase production indicate about a bacteria

A
  • it is likely be multi-drug resistant

- capable of sharing resistance mechanisms w/ other bacteria

120
Q

where do gram -ves tend to reside and how is this a serious issue for a px w/ CPO (carbapenemase-producing organisms)

A 
human bowel (w/ hundreds of millions of other bacteria) 
- px likely colonised for life
121
Q

what happens to a px that is colonised w/ CPO

A
  • isolated in a side room w/ contact infection control precautions
  • health care workers need to don PPE when providing physical care
122
Q

what is the most important example of the target site modification mechanism of antimicrobial resistance

A

flucloxacillin resistance in staph aureus resulting in MRSA

123
Q

outline the target site modification mechanism of beta lactam resistance

A
  • PBPs cross link peptidoglycan
  • beta lactams act on PBP
  • if change in PBP shape, beta lactam can’t bind
  • peptidoglycan cross linking continues
  • bacterium is resistant to beta-lactam
124
Q

outline how flucloxacillin resistance in staph aureus results in MRSA

A
  • in staph aureus, acquisition of mecA gene results in altered PBP called PBP2A
  • flucloxacillin can’t bind to PBP2A –> staph aureus resistant
  • now termed MRSA
125
Q

what are the treatment options of MRSA

A
  • clindamycin
  • vancomycin
  • Teicoplanin
126
Q

what happens to Px colonised w/ MRSA

A
  • isolated in a side room w/ contact precautions to prevent px-to-px spread of MRSA
127
Q

outline the restricted access mechanism of antimicrobial resistance

A

restricted access arises by:

  • antibiotic failing to get into bacterial cell due to loss of porins (access channels)
  • antibiotic being actively pumped out of bacterial cell due to ^ prod of efflux pumps
128
Q

why is restricted access antimicrobial resistance particularly problematic

A

can affect more than one antibiotic class

129
Q

give an example of bacteria w/ restricted access resistance and describe its resistances

A

pseudomonas aeruginosa

  • intrinsically resistant to most antibiotics
  • acquires resistance mechanisms –> MDR
  • most common mechanism is efflux pump
130
Q

what 6 drugs are active against pseudomonas aeruginosa

A
  • Piperacillin‐tazobactam
  • meropenem
  • ceftazidime
  • aminoglycosides
  • ciprofloxacin
  • aztreonam
131
Q

what is the only drug active against pseudomonas aeruginosa w/ restricted access

A

aminoglycosides

132
Q

why is antibiotic allergy documentation important

A
  • prevent life threatening drug reaction
  • avoid unnecessary drug restriction
  • antimicrobial stewardship
  • -> reduce use of ‘reserve’ antibiotics
133
Q

what is the most common antibiotic allergy

A

beta-lactams

134
Q

what is important to ask about when taking an allergy history

A

SEVERITY

  • time of onset, relative to dose
  • symptoms of evolution, duration
  • -> rash type:
    • maculopapular
    • urticarial
    • bullous
  • -> involvement of mucosal surfaces or internal organs
  • treatment required

DUE TO ANTIBIOTIC

  • exposure prior to reaction
  • other meds at time of reaction
  • antibiotic or relative tolerated since ?
  • other drug allergies
  • similar reaction in absence of drug ?
135
Q

what kind of allergic reactions are of major concern

A
  • have a fast onset
  • involve urticarial rash
  • include swelling e.g. of lips or tongue
  • breathing difficulties
  • required antihistamine treatment
136
Q

what is sepsis

A
  • life threatening organ dysfunction caused by disregulated host response to infection
  • interplay between host and pathogen
137
Q

why is sepsis important to treat quickly

A

chance of death ^ by 10% appx for every hour antibiotics delayed

138
Q

how to recognise sepsis

A
  • can use tools and scores
  • well known scores:
  • -> SOFA score from third international consensus definitions
  • sepsis screening tool from sepsis 6 (UK sepsis trust)

qSOFA (quick sequential organ failure assessment score) criteria:

  • resp rate >22
  • glasgow coma scale of 13 or less
  • SBP of 100 or less

(UK sepsis trust lists 10 features)

139
Q

what is crucial in sepsis investigation and why

A

identify the pathogen

  • ensures effective therapy
  • allows rationalisation of antibiotics
  • -> maintains antibiotic efficacy for next px
  • -> reduces collateral damage for px
140
Q

how can you identify the pathogen in sepsis

A

SEPTIC SCREEN

send samples; sample the tissues that you think are infected or inflamed

  • blood cultures (critical)
  • -> peripheral and central line if present
  • -> determine if px is bacteraemic (has replicating bacteria in blood)
  • urine culture
  • sputum culture
  • wound swab
141
Q

what is important to consider when choosing a suitable antibiotic for a potentially septic px

A
  • likely source of infection; any signs pointing towards particular anatomical source
  • what pathogens tend to cause infection in that site (is px known to be colonised w/ any resistant organisms)
  • known antibiotic allergies px
142
Q

what type of antibiotics tend to be used to treat sepsis

A

broad spectrum

GERR (46 decks)

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