Antimicrobial Chemotherapy Flashcards

1
Q

sensitive organism

A

organism is sensitive if it is inhibited or killed by the antimicrobial available at the site of infection

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2
Q

resistant organism

A

organism is resistant if it is not killed or inhibited by the antimicrobial available at the site of infection

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3
Q

bactericidal

A

antimicrobial that kills bacteria

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4
Q

bacteriostatic

A

antimicrobial that inhibits growth of bacteria - stops proliferation

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5
Q

M.B.C

A

Minimal bactericidal concentration = minimum concentration of antimicrobial needed to kill a given organism

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6
Q

M.I.C

A

Minimal inhibitory concentration = minimum concentration of antimicrobial needed to inhibit growth of a given organism

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7
Q

routes of administration of antibiotics

3 main ones

A
  • topical = applied to a surface (skin or mucous membranes)
  • systemic = taken internally (orally or parenterally)
  • parenteral = administered intra-venously (i.v.) or intra-muscularly (i.m.), occasionally subcutaneously
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8
Q

summarise bacteria classes: name examples for each

A

see sheet

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9
Q

mechanisms of action of antibiotics

name all 3

A

antibiotics may inhibit or kill bacteria by acting at 3 different areas of metabolic activity:
* inhibition of cell wall synthesis
* inhibition of protein synthesis
* inhibition of nucleic acid synthesis

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10
Q

classes of antibiotics to inhibit cell wall synthesis

A

Penicillins and Cepalosporins (B-lactams), Glycopeptides

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11
Q

what kind of antibiotics are those that inhibit cell wall synthesis

Penicillins, cephalosporins, glycopeptides

A

bactericidal

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12
Q

What are penicillins/celaphaloporins (b-lactams) and glycopeptides only effective against

A

gram positive bacteria: unable to penetrate g-ve cell wall

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13
Q

inhibition of cell wall synthesis- penicillins and cephalosporins (b-lactams)

just explain ahahah

A
  • effective mostly against gram-positive bacteria
  • beznyl penicillin= many gram-negative organisms resistant (inability to penetrate gram negative cell wall)
  • cephalosporins= second large group of b-lactam antibiotics
  • disrupt peptidoglycan synthesis by inhibiting the enzymes (penicillin-binding proteins, PBPs) responsible for cross-linking the carbohydrate chains
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14
Q

inhibition of cell wall synthesis- glycopeptides

A
  • inability to penerate gram-negative cell wall, they act only on gram-positive organisms
  • they act on cell wall synthesis at a stage prior to B-lactams, inhibitng assembly of a peptidoglycan precursor
  • they are not absorbed from the GI tract and are only given parenterally, except in special circumstances
    -e.g. vancomycin, teicoplanin
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15
Q

examples of glycopeptides

2

A
  • Vamcomycin
  • Teicoplanin
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16
Q

classes to inhibit protein synthesis

A
  • Aminoglycosides
  • Macrolides
  • Tetracyclines
  • Oxazolidinones
  • Cyclic Lipopeptide
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17
Q

inhibition of protein synthesis- aminoglycosides

A
  • Concentration-dependent bactericidal antibiotics
  • Useful in the treatment of serious Gram-negative infection (e.g. coliform)
  • Protein synthesis involves translation of messenger RNA at the ribosome and differences between the bacterial ribosome and the mammalian ribosome allow selective action on bacterial protein synthesis
  • Binding impairs translational proofreading leading to misreading of the RNA message, premature termination, or both, and so to inaccuracy of the translated protein product
    -e.g. gentamicin
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18
Q

example of amionglycoside

inhibits protein synthesis

A

gentamicin

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19
Q

what type of bacteria do aminoglycosides act on

inhibit protein synthesis

A

gram negative

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20
Q

inhibition of protein synthesis- macrolides

A
  • depending on concentration and bacterial species, bactericidal or bacteriostatic antibiotics
  • useful alternatives to penicillins in treatment of Gram-positive infections in patients who are penicillin allergic
  • Macrolides inhibit the bacterial protein biosynthesis, by preventing peptidyltransferase from adding the growing peptide attached to tRNA to the next amino acid as well as inhibiting ribosomal translation
    -e.g. erythromycin
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21
Q

Example of macrolide

inhibit protein synthesis

A

erythromycin

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22
Q

what class of bacteria do macrolides target

inhibit protein synthesis

A

gram-positive

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23
Q

what is a useful feature of erythromycin

Macrolide: inhibits protein synthesis

A

can be used to treat patients with a penicillin allergy

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24
Q

inhibition of protein synthesis- tetracylines

A
  • bacteriostatic antibiotics
  • treatment of gram-positive infections
  • Tetracycline inhibits protein synthesis by blocking the attachment of charged aminoacyl-tRNA to the A site on the ribosome. Tetracycline binds to the 30S and 50S subunit of microbial ribosomes. It prevents introduction of new amino acids to the nascent peptide chain
  • A significant percentage (10% or more) of Staph. aureus, Strep. pyogenes and Strep. pneumoniae strains are resistant.
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25
Q

what type of antibiotics are tetracyclines

inhibit protein synthesis

A

bacteriostatic

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26
Q

what type of bacteria do tetracyclines target

inhibit protein sysnthesis

A

gram-positive

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27
Q

what common strains of bacteria are resistant to tetracyclines

inhibit protein synthesis

A

s.aureus, strep.pyogenes, and strep. pneumoniae

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28
Q

inhibition of protein synthesis- oxazolidinones

A
  • Bacteriostatic or bactericidal antibiotics depending on bacteria being treated
  • treatment of gram-positive infections
  • can be given orally - held in reserve for treatment of serious infection
  • act as a protein synthesis inhibitor on the ribosomal 50S subunit of the bacteria- prevents the formation of the 70S initiation complex which is a prerequisite for bacterial reproduction
  • e.g. linezolid
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29
Q

what type of antibiotics are oxazolidinones

inhibit protein synthesis

A

Bacteriostatic or bactericidal antibiotics depending on bacteria being treated

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30
Q

why type of bacteria do oxazolidinones target

inhibit protein synthesis

A

gram-positive

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31
Q

example of oxazolidinone and when would it be used

A

linezolid: as a last resort/final option

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32
Q

inhibition of protein synthesis- cyclic lipopeptide

A
  • strong bactericidal antibiotics
  • treatment of gram-positive infections
  • Aggregation of daptomycin alters the curvature of the membrane, which creates holes that leak ions, causing rapid depolarization, loss of membrane potential, inhibition of protein, DNA, RNA synthesis, bacterial cell death
  • e.g. daptomycin
  • used for MRSA
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33
Q

what type of antibiotic is cyclic lipopeptide

inhibits protein synthesis

A

strong bactericidal antibiotic

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34
Q

what type of bacteria do cyclic lipopeptide target

inhibit protein synthesis

A

gram-positive

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35
Q

example of cyclic lipopeptide

inhibit protein synthesis

A

daptomycin: only used in really bad/resistant bacterial infection

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36
Q

what specific bacterial infection is daptomycin used to treat

cyclic lipopeptide: inhibits protein synthesis

A

MRSA

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37
Q

inhibitors of nucleic acid synthesis

A
  • Inhibition (different steps) in purine synthesis
  • Bacteriostatic, when combined, Bactericidal antibiotics
  • Inhibition of DNA synthesis either directly, or indirectly by interrupting the supply of precursors for DNA synthesis
  • e.g. trimethoprim, sulphamethoxazole, combined form in co-trimozaxole
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38
Q

Inhibitors of nucleic acid synthesis: Fluroquinolones

A
  • bactericidal antibiotics
  • particularly effective against **gram-negative **organisms inc pseudomonas
  • fluoroquinolones inhibit DNA synthesis more directly
  • used orally + parenterally
  • cannot be used in children due to interference with cartilage growth
  • e.g. ciprofloxacin, levofloxacin
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39
Q

examples of Fluroquinolones

inhibitors of nucleic acid synthesis

A
  • ciprofloxacin
  • levofloxacin
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40
Q

what type of antibiotic are fluroquinolones

inhibitors of nucleic acid synthesis

A

bactericidal antibiotics

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41
Q

what type of bacteria do fluroquinolones target

inhibitors of nucleic acid synthesis

A

gram-negative

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42
Q

When is an organism considered “resistant” to a drug

A

When it is unlikely to respond to attainable levels of that drug in tissues

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43
Q

3 types of antibiotic resistance

A
  • Inherent
  • Intrinsic
  • Aquired
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44
Q

what drug are gram-negative bacteria always resistant to

A

vancomycin

45
Q

acquired resistance

A
  • may be present in some strains but not others
  • Lab sensitivity testing required to establish sensitivity of any bacteria isolate from a patient
  • widespread use of antibiotics causes selective pressure and encourages new resistant organisms to outgrow sensitive strains

happens spontaneously

46
Q

inherint or intrinsic resistance

A

natural resistance to antibbiotic

laboratory sensitivty trsting is irrelevant in such cases

47
Q

how can antibiotic resistance be aquired and explain each

2 ways

A
  • spontaneous mutation: change in structure/function which no longer allows the antibiotic to act (target may have changed). happens spontaneously during DNA replication, DNA repair or DNA recombination
  • spread of resistance: genes that code for resistance can spread from organism to organism or from species to species. genes can be carried on plasmids or on transposons (packets of DNA which insert themselves into the chromosome). examples of horizontal gene transfer (new gene acquisition): conjugation (DNA transfer bacterial cells), transduction (bacterial DNA transferred by viruses- phage), transformation (naked DNA uptake by bacteria)
48
Q

B-lactamase production - what does it do and what commonly produces it

current issue in antibiotic resistance

A
  • β−lactamases are bacterial enzymes which cleave the β-lactam ring of the antibiotic and thus render it inactive
  • Most hospital strains of Staphylococcus aureus produce β-lactamase
  • β-lactamases are also common in Gram-negative bacilli
49
Q

2 ways to combat B-lactamase

give examples

A
  1. modify the antibiotic side chain producing
    new antibiotic resistant to the actions of β-lactamase - co-amoxiclav= amoxicillin plus the β-lactamase inhibitor clavulanic acid
  2. introduce a second component to the antibiotic (β-lactamase inhibitor) protecting the antibiotic from enzymatic degradation -flucloxacillin= (antistaphylococcal) which is a modified form of penicillin
50
Q

Extended spectrum β-lactamases (ESBLs)

probs don’t need to know - maybe learn what they are…

A

Enzymes that mediate resistance to extended-spectrum (third generation) cephalosporins

  • Antibiotic resistance transferred by conjugation (plasmids)
  • Problem in hospitals by some Gram-negative organisms
  • E.S.B.L. carrying organisms selected infection control measures in place to stop such organisms passing from patient to patient
51
Q

Carbapenemase-Producing Enterobacteriaceae (CPE)/Carbapenem Resistant Enterobacteriaceae (CRE) - issue with antibiotic resistance

not sure if need to know?

A
  • emerging clinical problem
  • Extremely resistant Gram-negative organisms to the carbapenems
  • Similar to penicillins and cephalosporins, carbapenems are members of the β- lactam class of antibiotics
  • In some cases NO antimicrobial options for therapy
  • CPE now endemic in healthcare facilities in many countries
  • Infection prevention and control measures to prevent patient to patient spread in the hospital setting.
52
Q

Alteration of penicillin binding protein (PBP) target site

issue with antibiotic resistance

A
  • Micro-organisms develop resistance to β-lactams by changing the structure of their PBPs
  • Mutations in PBP genes result in a modified target site to which β-lactams will no longer bind
  • ex; methicillin resistant S. aureus (MRSA)
53
Q

what is MRSA

A

any strain of S. aureus that has developed, through horizontal gene transfer and natural selection, multiple drug resistance to β-lactam antibiotics

54
Q

what drugs can be used to treat MRSA

A

daptomycin, vancomycin, linezolid

Not flucloxacillin which is used for B-lactamase resistance

55
Q

glycopeptide resistance Vancomycin - (in relation to MRSA?)

issue with antibiotic resistance

A
  • Resistance to vancomycin among Gram-positive organisms
  • Glycopeptides could be relied on for the treatment of serious Gram-positive infection but recently vancomycin resistant enterococci have emerged-
    (Enterococcus faecalis and Enterococcus faecium)
    In Vancomycin Resistant Enterococci (VRE),
    the peptidoglycan precursor to which vancomycin normally binds has an altered structure
    this mechanism of resistance might spread from enterococci to S. aureus, producing vancomycin resistant S. aureus
56
Q

commonly used agents: B-lactams - penicillins

6: explain each

A
  • benzyl penicillin (penicillin G): used for gram-positive organisms e.g. intravenous treatment of pneumococcal, meningococcal and Strep. pyogenes infection
  • amoxicillin, ampicillin: for gram-negative activity, 20-30% of coliforms now resistant, oral absorption, covers streptococci and some coliforms
  • co-amoxiclav: B-lactamase producing coliforms
  • flucloxacillin: used for staphylococcal infections, resistant to staphylococcal β-lactamase action, similar agent to methicillin
  • piperacillin: used for extended gram-negative cover, activity against enterococcus faecalis and pseudomonas, anti-aerobic activity (intra-abdominal infection), combination with the B-lactamase inhibitor tazobactam
  • imipenem, meropenem: active against most bacteria, including anaerobes, close relatives of the penicillins
57
Q

B-lactams: Cephalosporins - explain G+ve and G-ve activity

A

-gram-negative activity (increases through generations)
-gram-positive activity (decreases proportionately from first through to third generation drugs)

58
Q

aminoglycosides

action against? example…

A

-action against gram-negative organisms
-most staphylococci sensitive but not streptococci
-e.g. gentamicin
-serum levels must be monitored because of potential toxicity

59
Q

glycopeptides

active against… examples

A

-activity only against gram-positive organisms both aerobic and anaerobic
-e.g. vancomycin (levels must be monitored because of potential toxicity), teicoplanin

60
Q

macrolides

active against

A

-clarithromycin or erythromycin activity mainly against gram-positive organims
-used as alternative to penicillin in patients with penicillin hypersensitivity
-e.g. clarithromycin, erythromycin (effective against organisms causing ‘atypical pneumonia’), azithromycin (for chlamydia)

61
Q

quinolones

active against… examples

A

-wide spectrum of action
-active against nearly all gram-negative organisms including pseudomonas infections
-can be used against staphylococci and pseudomonas infections
-e.g. nalidixic acid, ciprofloxacin, levofloxacin

62
Q

miscellaneous agents

just name and describe a bunch - probs best to not bother learning

A
  • metronidazole= effective against anaerobes- gram positive e.g. clostridia, gram-negative e.g. Bacteroides spp, resistance against anaerobes virtually unknown
  • trimethoprim (nucleic acid synthesis inhibitor)= treatment of urinary infections co-trimoxazole (trimethoprim + sulphamethoxazole)=Used for a few specialised conditions and sometimes for treatment of chest infections on the grounds that it does not predispose to Clostridium difficile infection
  • fusidic acid= used only as an anti-staphylococcal drug, Stap. aureus can develop resistance very readily to this agent, it should always be used in combination with other anti-staphylococcal drugs (i.e. flucloxacillin), it diffuses well into bone and tissues and so is useful in staphylococcal osteomyelitis and pneumonia
  • tetracyclines= Broad spectrum agents which inhibit bacterial protein synthesis and have a few limited applications nowadays, useful for some genital tract (chlamydia) and
    respiratory tract infection (e.g. psittacosis, Mycoplasma pneumoniae), should not be given to pregnant women or children under 12 years of age as they are deposited in teeth and bone
    clindamycin= The only lincosamide antibiotic in common use and has good activity against Gram-positive organisms such as staphylococci and streptococci, good activity against anaerobes, very good tissue penetration e.g. into bone, can be taken orally, common cause of pseudo-membraneous colitis
63
Q

linezolid

what is it active against, and what is a good feature of it

A

-activity against MRSA
-can be given orally unlike glycopeptides
-can cause bone marrow suppression

64
Q

daptomycin

active against, when is it useful

A

-active against gram-positive organisms only
-may be useful for treatment of serious MRSA infections

65
Q

agents only used in the treatment of lower urinary tract infection (cytisis)

give 2 and explain action…

A
  • nalidixic acid (quinolone)= urinary. antiseptic with activity only against gram-negative aerobes (coliform) organisms, completely excreted in urine
  • nitrofurantoin (quinolone)= effective against most gram-negative organisms (not proteus and pseudomonas spp.) effective against some gram-positive organisms
66
Q

what is incidence of antibiotic side effects dependent upon

A

dose and duration of therapy

67
Q

what are the majority of antibiotic side effects like

A

trivial and reversible upon withdrawal of the antimicrobial - however some are severe of fatal

68
Q

examples of antibiotic side effects

about 9 and maybe try to describe a few of these effects -is LO so learn

A
  • allergic reactions
  • immediate hypersensitivity - anaphylactic shock
  • delayed hypersensitivity - immune complexes or cell mediated mechanisms
  • gastrointestinal side effects - nausea/vomiting
  • thrush - disrupt normal microbial flora
  • liver toxicity
  • renal toxicity
  • neurological toxicity
  • haematological toxicity
69
Q

how can we minimise adverse reactions to antibiotics

A

antimicrobials should be used only when indicated and in the minimum dose and duration necessary to achieve efficacy, care should be taken when administering antimicrobials to susceptible groups e.g. old/young, pregnant women, patients with liver/renal insufficiency

should be monitored to ensure maximal efficacy and minimal toxicity

70
Q

usage of antimicrobial agents - considerations to be made

A
  • balance to be struck between needs of the individual patient and possible impact on others of increased antimicrobial resistance or emergence of C diff as a result of treatment
  • should not be prescribed unless absolutely necessary
  • considerations to be aware of in choosing right agent
71
Q

factors to consider when choosing antimicrobial agent

A
  • age= some drugs contraindicated in children
  • renal function= many antimicrobials excreted by kidneys, accumulate in the body when there is renal failure
  • liver function= antimicrobials can be metabolised by the liver and excreted in bile, doses should be decreased in hepatic insufficiency
  • pregnancy= some antimicrobials contraindicated in pregnancy, mutagenic (induce mutation in foetal chromosomes), tetratogenic (associated with congenital abnormalities
    or both (e.g., metronidazole and trimethoprim))
72
Q

antimicrobials safe in pregnancy

A

penicillins, cephalosporins,urinary antiseptic nitrofurantoin

73
Q

indication for antimicrobials: prophylaxis

what is it, and what are some common things to take into account…

A

administration of antimicrobials to prevent the future occurrence of infection

patient exposed to other patients with highly communicable disease or about to have surgery with high post-operative infection rates, most abdominal operations, dosage should only cover period of risk

74
Q

indication for antimicrobials - therapy

A

if organism causing infection not known, empirical antimicrobial therapy should be commenced if urgent treatment required

should take site and type of infection into account as well as causative organisms and their common antimicrobial susceptibility patterns, treatment prescribed should be reviewed once results of culture and antibiotic sensitivity tests become available

75
Q

drug realated considerations - spectrum of antimicrobial agent

A

antibiotic chosen should normally be effective against known or likely causative organism - ideally choice based on results of sensitivity test

76
Q

drug related considerations - monotherapy vs combination

A

useful to cover mixed infection by more than one organism, because 2 antimicrobials sometimes have an enhanced effect together, to minimise the development of resistant strains to any one agent

77
Q

possible outcomes when antimicrobials are used in combination

3

A
  • their effects can be addictive
  • they may be antagonistic and have a combined effect which is less than the sum of their individual contributions
  • they may be synergistic and have a combined effect which is greater than the sum of their individual contributions

e.g. combination of penicillin and gentamicin for streptococcal infective endocarditis

78
Q

combination of 2 cidal and 2 static drugs

A

generally additive or synergistic

79
Q

combination of 1 static and 1 cidal drug

A

may result in antagonism

80
Q

drug related considerations - penetration to site of infection

A

antimicrobial with high serum concentrations, appropriate spectrum and excellent safety profile, but unable to penetrate to the site of infection is of little use in clinical practice

81
Q

drug related considerations - monitoring

A

gentamicin and vancomycin have low therapeutic index, difference between therapeutic and toxic dose is small

82
Q

drug related considerations - dose and duration of therapy

A

patients with serious infections often require much higher dosages, the use of drug combinations may further influence dosage

83
Q

list all 5 drug related considerations

A
  • spectrum of antimicrobial agent
  • monotherapy vs combination
  • penetration of site of infection
  • monitoring
  • dose and duration of therapy
84
Q

role of the laboratory (and clinical microbiologists) in choice of antibiotics

is LO so learn

A
  • advice on choice of antimicrobial - identify organism and do antibiotic sensitivity test
  • dosage and duration of therapy - pateint’s age, size, renal function, motitoring of efficacy and toxicity should be taken into account
85
Q

why are serum levels of an antimicrobial monitored

A
  1. to ensure that therapeutic levels have been achieved
  2. to ensure that levels are not so high as to be toxic - antibiotics most commonly measured in serum are gentamicin and vancomycin
86
Q

simplest way to measure M.I.C of one antibiotic agaist one organism (susceptibility testing)

minimum inhibitory concentration

A

using E-test, paper strip with antibiotic conc absorbed into it, can be read directly from the point where organism growth intersects the strip

min conc required to inhibic bacterial growth

87
Q

automated methods of testing - sisceptibility testing

A
  • growth of individual isolates measured and presence of different conc of each antibiotic and M.I.C. calculated (determine if organism is “sensitive” or “resistant”
  • results only give a prediction of whether the infection is likely to be cured by the antibiotic in question
88
Q

factors to influence susceptibility testing

A
  • route of administration
  • dosing schedule
  • penetration of antibiotic to the taget site and interactions with other drugs
  • (e-test)
89
Q

do antibiotics have an action on fungi or fungal infection

and what does?

A

have no action: anti-fungal drugs used instead

90
Q

how can fungi be subdivided

2 ways

A
  • yeasts
  • dilamentous fungi (moulds)
91
Q

classes of anti-fungal drugs

A
  • polyenes
  • azoles
  • allyamines
  • echinocandins
92
Q

polyenes (anti-fungal drugs)

mechanism of action, effect on fungal types, examples

A
  • bind to ergosterol, present in the fungal cell wall but not in the bacterial cell wall, and this results in an increase in the permeability of the cell wall
  • active against yeasts and filamentous fungi
  • also bind to other sterols e.g. cholesterol in mammalian cell membranes=> their toxicity
  • e.g. amphotericin B= intravenous use, treatment of serious systemic fungal infection, extremely toxic, resistance unusual
  • e.g. nyastin= topical use only e.g. in creams, for fungal skin infections, in pessaries for vaginal candida infections, oral suspension for oral and oesophageal candidiasis
93
Q

azoles (anti-fungal drugs)

mechanism of action, effect on fungal types, examples

A
  • inhibition of ergosterol synthesis
  • triazoles= fluconazole- oral and parenteral treatment of yeast infections, itraconazole- active against yeast and filamentous fungi, voriconazole- treat aspergillosis
  • imidazoles- miconazole, ketoconazole
94
Q

allylamines (anti-fungal drugs)

mechanism of action, effect on fungal types, examples

A
  • suppress ergosterol synthesis
  • act at diff stage of synthetic pathway from azoles
  • only allylamine in common use= terbinafine
  • active against dermatophyte infections of skin e.g. athlete’s foot and nails
  • mild infections treated topically and more serious infections orally
95
Q

echinocandins (anti-fungal drugs)

mechanism of action, effect on fungal types, examples

A
  • inhibit synthesis of glucan polysaccharide in fungi
  • used for serious candida and aspergillus infections
  • e.g. caspofungin, micafungin, anidulafungin
96
Q

what action do antibiotics have against viruses

A

no action

97
Q

antibiotic

A

compounds that block the growth and reproduction of bacteria

98
Q

what kind of agents are all anti-viral drugs

A

no virucidal agents (kill virus) but all virustatic agents (inhibit growth and/or replication)

99
Q

what are many anti-viral drugs

A

nucleoside analogues which interfere with nucleic acid synthesis

100
Q

types of anti-viral drugs - what viruses can they target

A
  • anti-herpes virus drugs
  • anti-HIV drugs
  • drugs for chronic hepatitis B and C
  • drugs for viral respiratory infections
101
Q

anti-herpes virus drugs

idk, just explain them and give examples…

A
  • treatment most effective if started early but doesn’t eradicate any of these viruses
  • aciclovir= active against herpes simplex virus and varicella zoster virus, nucleoside analogue, must be converted to active form by thymidine kinase coded for by the virus genome, specific for virus-infected cells, very low toxicity for uninfected host cells
  • valaciclovir, famaciclovir= oral agents, treatment of HIV and shingles
  • valganiciclovir= bone marrow toxicity, pro-drug of ganciclovir, oral,
  • foscarnet= used for some HSV, VZV and CMV that are resistant to nucleoside analogues, highly nephrotoxic (should only be given intravenously)
  • cidofovir= used for CMV retinitis when other anti-viral drugs inappropriate
102
Q

anti-HIV drugs

idk, just explain them and give examples…

A
  • combination therapy normal practice in HIV treatment (normally 3)
  • drugs active on at least 2 different stages of HIV replication
  • 2 nucleoside analogue reverse transcriptase inhibitors, plus either non-nucleoside reverse transcriptase inhibitor or viral protease inhibitor
  • zidovudine= nucleoside analogue interfering with action of reverse transcriptase, high incidence of side effects such as anaemia and neutropenia
  • ex; nevirapine and saquinavir
103
Q

drugs for chronic hepatitis B and C

idk, just explain them and give examples…

A
  • interferon-a= produced by genetic engineering, used to treat selected chronic hep B and C infections, low response rate, serious side effects, high cost of treatment
  • ribavirin= treatment for chronic hep C, can be given orally
  • adefovir dipivoxil, lamivudine= HIV treatment, hep B, can be given orally (advantage over interferon-a)
104
Q

drugs for viral respiratory infetions

idk, just explain them and give examples…

A
  • zanamivir, oseltamivir= treatment of influenza A or B
  • ribavirin= treatment of severe respiratory syncytial virus infections, must be inhaled, administration difficult, reduces mortality in Lassa fever, used in combination treatment for chronic hep C
  • remedesivir= treatment of COVID-19, adenosine nucleotide triphosphate analogue- interferes with action of viral RNA-dependent RNA polymerase
105
Q

anti-viral resistance

A
  • testing viruses for resistance only available in a few drugs
  • genotypic analysis (i.e., sequencing of part of the viral genome) may help in choosing rational treatment in selected patients
106
Q

anti-viral drug levels

A
  • only available for a few drugs (e.g. some anti-HIV drugs and aciclovir)
  • drug monitoring done to ensure therapeutic but not toxic serum levels achieved (for aciclovir this is usually restricted to patients with significant renal impairment)
107
Q

significant resistance mechanism for particular groups
of drugs

most common one

A

B-lactam ring resistance (B-lactamase) by some bacteria

108
Q

common factors to consider in choosing suitable antimicrobial agents to prevent or treat infection

Idk made it up from the LO, not sure if in lectures - kinda common sense

A

G-positive or G-negative, B-lactam, antibiotic resistance in areae, severity of infection, nature of infection (e.g. widespread or localised), have other been used and failed…