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Principles of antimicrobial use Flashcards

1
Q

What is an infection?

A

organism/pathogen invades host tissues and elicit inflammatory/immune host responses

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2
Q

What is sepsis?

A

life-threatening organ dysfn caused by dysregulated host response to infection

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3
Q

What are the 4 things in a systemic approach to antimicrobial use?

A
  1. Confirm presence of infection
  2. Identify likely pathogens
  3. Select antimicrobial agents and regimen
  4. Monitor response
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4
Q

Which 2 steps fall under indication for Abx?

A
  1. Confirm presence of infection

2. Identification of (likely) pathogens

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5
Q

Which step falls under the ‘regimen (choice, route, dose, duration)’

A

Step 3: Selection of antimicrobial and regimen

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6
Q

Which step falls under the ‘monitoring and plan’?

A

Step 4: Monitor response

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7
Q

How to confirm presence of infection?

A

a. Any risk factors for infection
b. subjective evidence
c. objective evidence
d. Possible site of infection

  • looking for diagnosis
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8
Q

What are 4 risk factors to look at for infection?

A
  • Disruption of natural protective barriers (innate immunity)
  • Age
  • Immunosuppression
  • Alterations in normal flora of the host with conditions that promotes overgrowth of MO
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9
Q

What to look at for subjective evidence?

A
  • Localised symptoms (diarrhoea, N/V, dysuria, pain, purulent discharge)
  • Systemic symptoms (feverish, SOB, weakness/tiredness, etc.)
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10
Q

What to look at for objective evidence?

A
  • Vital signs (Fever, Hypotension, Tachypnoea, HR, Mental status)
  • Lab test (non-specific biomarkers, acute-phase reactants)
  • Radiological imaging

CONSIDER TREND; baseline VS current values

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11
Q

Guidelines for starting of ABx: When procalcitonin levels are?

A

> = 0.5 ug/L: ABx encouraged

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12
Q

Guidelines for continuing of ABx: When procalcitonin levels are?

A

decrease by 80% from peak concentration; and >= 0.5 ug/L: Continue Abx

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13
Q

Guidelines for stopping of ABx: When procalcitonin levels are?

A

< 0.5 ug/L: Stop Abx

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14
Q

How do we find the possible site of infection?

A
  • Clinical presentation
  • Risk of infections
  • O and S evidence
  • Common sites are UTI, Resp tract, soft tissues, intra-abdominal
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15
Q

What is considered a pathogen?

A

Organisms capable of damaging host tissue and eliciting a host response and signs and sx of an infection

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16
Q

What is a coloniser? Example?

A

Presence of normal flora/pathogenic organisms without eliciting a host response

e.g. yeast from urine culture

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17
Q

What is a contaminant?

Example?

A

Presence of MO typically acquired during collection/processing of host specimens w/o evidence of host response

e.g. S. epidermidis (from skin) + bacillus spp.

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18
Q

What is empiric therapy? and when to use empiric therapy?

A
  • When micrological results are unavailable
  • Clinical presentation of likely site of infection
  • Likely susceptibility
  • Antibiogram
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19
Q

What is definitive therapy? and when to use definitive therapy?

A
  • Culture-directed therapy

- based on pts specific microbiological (culture and susceptibility tests)

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20
Q

What is prophylaxis therapy? and when to use prophylaxis therapy?

A
  • Abx given to prevent infection

e. g. surgical prophylaxis; post-exposure prophylaxis

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21
Q

Benefits of combination therapy?

A
  • Extend spectrum of activity
    e. g. pip-tazo + vancomycin (covers MRSA) for HA-pneumonia
    e. g. pip-tazo + ciprofloxacin (to broaden; cover p.aeruginosa) for VA-pneumonia
  • Achieve synergistic bactericidal effect (however, note that indifference/antagonism happens too)
    e. g ampicillin + gentamicin or amipicllin + ceftriaxone for enterococcus endocarditis
  • Prevent development of resistance
    e. g. TB treatment
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22
Q

Limitations of combination therapy?

A
  • Inc toxicity and allergic rxns
  • Inc risk of DDI
  • Inc cost
  • Selection of MDR bacteria
  • Inc risk of superinfections
  • Concern for antagonistic effect (VS synergisitc)
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23
Q

What are some host factors to consider when choosing the ABx?

A
  • Age
  • G6PD def
  • History of allergies and ADR
  • Cross-reactivity btw penicillins and other b-lactams
  • Preg/lactation
  • Renal/hepatic impairment
  • Status of host immune fn (use bactericidal drugs for immunocompromised + combination therapy as more vulnerable to polymicrobial infection)
  • Severity of illness
    (may need broader spectrum e.g. covering Pseudomonas)
  • Recent Abx use
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24
Q

What are some drug properties to consider when choosing the ABx?

A
  • Active against suspected organism
  • Ability to reach site of infection (CNS penetration)
  • PK-PD
  • ROA
  • Side effects
  • DDI
  • Cost
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25
Q

Enterobacteriacea VS Enterobacterales

A

Family VS Order

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26
Q

Different route of administrations

A

IV, IM, PO, intrathecal, inhalation, topical

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27
Q

When is IV route used?

A

hospitalised, severe infections, when high blood conc is required

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28
Q

Why is oral the preferred route?

A

IV needle can also cause infection; for the comfort of the patient
Less invasive and less nursing time
Oral prevents irritation to vein/ occur blood stream infections

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29
Q

When is oral route not used?

A
  • Absorption problem (GI pathology)
  • Suitable oral ABx unavailable
  • High tissue conc essential (e.g. meningitis, endocarditis, bone/joint)
  • Urgent treatment required
  • Patient non-compliance
30
Q

ABx example with good oral F

A
  • FQs
  • metronidazole
  • linezolid
  • co-trimoxazole
31
Q

Advantages of using IV ROA?

A
  • higher ABx conc, more reliable levels, for pts unable to abs orally (100% F)
32
Q

Disadvantages of using IV ROA?

A
  • Need IV access
  • Hospital administration
  • Phlebitis
  • Cost
33
Q

Why is IM less commonly used?

A

Painful
Only for community based
e.g. Streptomycin, Ceftriaxone, Benzathine penicillin

34
Q

When is aerosolised/nebulised used?

A

Nebulised colistin for MDR resistant P. aeruginosa pneumonia

35
Q

What are some drug side effects/ADR we need to consider?

A
  • cdad
  • collateral damage

Ecological adv effects when selecting organism and colonisation of MDR
Not only with the Abx but also other Abx

36
Q

What are some DDI PK-PD we need to consider?

A
  • CYP450 inhibitors (e.g. azole antifungals, macrolides)
  • CYP450 inducers (e.g. rifampicin)
  • Carbapenems and valproate NOT USED TOGETHER
  • cross-reactivity with penicillins with other b-lactams
37
Q

The cost of drug includes:

A

acquisition, preparation, administration, monitoring

38
Q

What is a treatment goal?

A
  • When you achieve therapeutic response

- Lack of ADR

39
Q

What is a therapeutic response?

A
  • Resolutions of S&S (the subjective and objective should be resolved)
  • Microbiological clearance - eradication of organism
  • Absence of complications/progression
40
Q

What are some ADR that occurs in new ABx?

A

Rashes, itch, angioedema

41
Q

When do we modify therapy?

A
  • When susceptibility/microbiologic tests becomes available (optimise therapy: escalate or de-escalate)
  • Satisfactory response (Convert IV to Oral; De-escalate/streamline from broader to narrower spectrum Abx; Stop if completed adequate duration)
  • Unsatisfactory response
42
Q

What are the causes of unsatisfactory response?

A
  • Inappropriate diagnosis (could be fungal/viral)
  • Inappropriate choice of agent (resistance develop)
  • Subtherapeutic conc (non-compliance, improving renal fn, DDI)
  • Collections or abscess - needs surgery or drainage
  • Impaired host defense
  • Superinfection
  • Toxicity of the drug
43
Q

How long to wait to evaluate clinical response?

A

48-72hours

44
Q

what Abx we avoid in children

A

FQs (anthropathy), tetracyclines (discolor teeth)

45
Q

what Abx to avoid in G6PD deficiency

A

sulfonamides (co-ts), Nitrofurantoin, ?FQs

46
Q

which B lactam doesnt have any cross reactivity with the other B lactams

47
Q

what are some examples of possible cross reactivity of B lactams?

A
  1. amoxicillin and ampicillin
  2. amoxicillin/ampicillin with cephalexin
  3. cefepime and ceftriaxone
  4. ceftazidime and aztreonam
48
Q

which abx are safe in preg

A

B lactams, macrolides

49
Q

abx to avoid in preg

A

FQs, Co-TS, tetracycline

50
Q

what abx cause nephrotoxicity

A

AGs, high dose vancomycin

51
Q

what abx cause hepatotoxicity

A

pyrazinamide, augmentin

52
Q

what are bactericidal abx

A

B lactams, quinolones, AGs, vancomycin

53
Q

abx to treat CNS infections

A

penicillin, ceftriaxone, cefepime, ceftazidime, meropenem, vancomycin

54
Q

abx that dont concentrate in CSF

A

1 and 2 cephalosporins, AGs, macrolides, clindamycin

55
Q

abx covering ESBL producing enterobacterales

A

4th gen cephalosporins, carbapenems

56
Q

abx covering Amp-C producing enterobacterales

A

4th gen cephalosporins, carbapenems

57
Q

abx covering anaerobic

A

augmentin, carbapenem, pip-tazo, metronidazole

58
Q

abx which are concentration-dependent kill

59
Q

what is concentration-dependent bactericidal killing

A
  • higher conc results in more rapid and more extensive killing
  • optimise peak: MIC ratio (where the peak is 8-10x above MIC)
  • ciprofloxacin 500mg Q24H better than 250mg Q12H
60
Q

rationale behind once-daily dosing of AGs (for conc-dependent killing)

A
  1. post-abx effect
  2. prevents adaptive resistance –> prevents selection of more resistant mutants
  3. less nephrotoxicity
  4. lower cost
61
Q

how do we change dose interval for conc-dependent killing?

A

hartford nomogram

CrCL:
>= 60 -> 24H
40-59 -> 36H
20-39 -> 48H

or based on graph
concentration:
<7.5 = Q24H
7.5-11 = Q36H
>11 = Q48H
62
Q

what is the abx that falls under time-dependent bacterial killing with no persistent effect (short half live)

A

B lactams (pen, cephalosporins, carbapenems)

63
Q

what is time-dependent bacterial killing with no persistent effect (short half live)

A

amt of time the abx conc is above the MIC of organism

64
Q

dosing strategies for

time-dependent bacterial killing with no persistent effect (short half live)

A

-%time > MIC (40-70% dosing interval above MIC)

  • more freq dosage administration
  • continuous IV infusion or prolonged intermittent infusion
  • block excretion by giving probenecid
65
Q

what abx fall under time-dependent bacterial killing with persistent effect (long half live or post-abx effect)

A

vancomycin

66
Q

what is time-dependent bacterial killing with persistent effect (long half live or post-abx effect)

A

rate and extent of bacterial killing related to AUC vs MIC

67
Q

what is the dosing strategy for time-dependent bacterial killing with persistent effect (long half live or post-abx effect)

A

optimise AUC: MIC ratio (vancomycin: target 400-600 for MRSA)

  • dependent on TOTAL DAILY DOSE
    e. g. 500mg Q12H or 1g Q24H –> we give the 1g q24h as IV injection given once
68
Q

ADR in AGs and vancomycin

A

AGs: serum creatinine, urine output
vancomycin: flushing, hypotension, itch

69
Q

what to take note about daptomycin

A

not used in pneumonia as daptomycin is inactivated by lung surfactant

70
Q

what to take note with AGs

A

less effective in abscesses

71
Q

which gram -ve bacteria can produce Amp-C beta-lactamase?

A
  • Enterobacter
  • Citrobacter freundii
  • Providencia
  • Proteus vulgaris
  • Morganella
  • Serratia

these may develop resistance against 3rd gen cep

72
Q

what are 2 examples of superinfections?

A

Second infection superimposed of the first infection:

1) Clostridioides Difficle (cause kill the susceptible microbes alr
(2) Fungal infections

PT (19 decks)

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