Antimicrobials in clinical practice Flashcards

1
Q

Dental abscess antibiotics

A

Amoxicillin 500mg tds x 5/7
Or
Penicillin V 500mg qds x 5/7

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2
Q

Considerations when giving antibiotics

A

Are antibiotics necessary?
What is the site of infection?
What is the organism sensitivity?
What is the appropriate or available route of administration?
What antibiotics are safe for the patient?

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3
Q

Are antibiotics necessary?

A

Is there a non antibiotic option?
Is there evidence of infection?
Is there evidence of a bacterial infection?
Is the bacteria colonising or actually causing disease?

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4
Q

Dental abscess - primary management

A

pulpectomy / incision and drainage
analgesia
The addition of antibiotics is not recommended for a localized dental abscess.

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5
Q

Dental abscess- antibiotics indicated if

A

No possibility of immediate attention by a dental practitioner,
Or
Features of severity / increased risk …

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6
Q

Features of severity or increased risk

A

Signs of severe infection e.g. fever, lymphadenopathy, cellulitis, diffuse swelling.
Systemic symptoms e.g. fever or malaise.
A high risk of complications e.g. people who are immunocompromised or diabetic or have valvular heart disease.

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7
Q

Is it a dental abscess? **

A

Evidence of infection?

Obtain a blood culture
(aerobic and anaerobic) before initiating parenteral antibiotics.
Needle aspirate is indicated for Gram stain and aerobic and anaerobic culture

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8
Q

Dental abscess - differential diagnosis

A
NON-INFECTIOUS
Localized lymphadenopathy due to other infection or a neoplasm.
Salivary gland problem due to stone, infection (parotitis), or dehydration/dry mouth.
Neoplasm: 
-intraoral.
-salivary gland.
Unerupted teeth
VIRAL: mumps
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9
Q

What is the site of infection?

A

What organisms should be covered?

Which antibiotics will penetrate that site?

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10
Q

Pharyngitis vs dental abscess

A
Pharyngitis: Streptococcus pyogenes
EBV
Dental abscess:
Viridans group streptococci
Anaerobes
Gram negative rods
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11
Q

Bacteria associated with dental infection

A
Bacteroides
Fusobacterium
Actinomyces
Peptostrep
P. melaninogenica
S. viridans
S. aureus
Haemophiius
T. spp.
(know gram and an/aero)
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12
Q

Antimicrobials and oral infections: penicillin

A

S. sanguis (viridans)
N. gonnorhoeae
T. spp.
Anaerobes +/-

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13
Q

Antimicrobials and oral infections: Flucloxacillin

A

S. aureus

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14
Q

Antimicrobials and oral infections: Ampicillin

A
S sanguis (viridans)
N. gonnorhoeae
H. influenzae (+/-)
T. spp
Anaerobes +/-
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15
Q

Antimicrobials and oral infections: Cefuroxime

A
S sanguis (viridans)
S. aureus (+/-)
N. gonnorhoeae
H. influenzae
T. spp
Anaerobes +/-
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16
Q

Antimicrobials and oral infections: clindamycin

A

S sanguis (viridans)
S. aureus
Anaerobes

17
Q

Antimicrobials and oral infections: erythromycin (macrolides)

A

S sanguis (viridans)
S. aureus (+/-)
H. influenzae (+/-)

18
Q

Antimicrobials and oral infections: Gentamicin

A
S sanguis (viridans)
S. aureus (+/-)
N. gonnorhoeae
H. influenzae
T. spp.
19
Q

Antimicrobials and oral infections: metronidazole

A

Anaerobes ++

20
Q

Primary and acquired resistance

A

Primary Resistance
-innate property e.g. Pseudomonas and penicillin
Acquired Resistance
-due to mutation or gene transfer
-chromosomal e.g. M.tuberculosis, plasmid mediated e.g. MRSA

21
Q

How do bacteria resist antibiotics?

A

Change antibiotic target
Destroy antibiotic
Prevent antibiotic access
Remove antibiotic from bacteria

22
Q

How does resistance develop?

A

Intrinsic - naturally resistant
Acquired
-spontaneous gene mutation
-horizontal gene transfer –> conjugation, transduction, transformation

23
Q

How do we detect resistance/ sensitivity?

A

Antibiotic sensitivity testing
Breakpoint plates
Chromogenic plates
Mechanism-specific tests e.g. detection of beta-lactamases
Genotypic methods such as PCR for known resistance conferring genes e.g. Rifampicin resistance probe

24
Q

Antibiotic sensitivity testing

A

Dilutional liquid culture MIC and MBC
Antibiotic discs
E-tests

25
Breakpoint plates
plates with a specific 'breakpoint' concentration of antibiotic in and see if a given inoculum grows or not
26
Lowest MIC
Does not necessarily mean best antibiotic Also consider -pharmacokinetics, -protein binding -distribution into the site of infection, -exposure of an organism to an antibiotic needed for its eradication
27
Antimicrobials are molecules that work by binding target site on bacteria
Defined as points of biochemical reaction crucial to the survival of the bacterium -penicillin-binding proteins in cell wall -cell membrane -DNA -Ribosomes -Topoisomerase IV or DNA gyrase Crucial binding site will vary with the antibiotic class
28
Antibiotic must bind to target site(s) in bacterium
Penetrate outer membrane (penetration resistance), Avoid being pumped out of the membrane (efflux pump resistance), Binding site can change its molecular configuration Remain intact as a molecule (e.g., avoid hydrolysis by beta-lactamases)
29
Drug must not only attach to its binding target but also
must occupy an adequate number of binding sites, which is related to its concentration within the microorganism
30
To work effectively, the antibiotic should
remain at the binding site for a sufficient period of time in order for the metabolic processes of the bacteria to be sufficiently inhibited.
31
Two major determinants of bacteria killing include
concentration and the time that the antibiotic remains on these binding sites
32
Concentration-dependent killing
Key parameter is how high the concentration is above MIC Peak conc / MIC ratio -aminoglycosides -quinolones
33
Time dependent killing
Key parameter is the time that serum concentrations remain above the MIC during the dosing interval: t>MIC -beta-lactams (penicillins, cephalosporins, carbapenems, monobactams), -clindamycin, -macrolides (erythromycin, cla rithromycin), -oxazolidinones (linezolid),
34
What is the appropriate or available route of administration?
And dosage interval/ duration | e.g. Strep pharyngitis: Penicillin V, oral, 6 hourly, 10 days
35
What antibiotics are safe for the patient?
- intolerance, allergy and anaphylaxis - side effects - age - renal function - liver function - pregnancy and breast feeding - drug interactions - risk of Clostridium difficile (5 ‘C’s)
36
Risk of C. difficile
``` 5 Cs Ciprofloxacin Clindamycin Cephalosporins Co-amoxiclav (augmentin) Carbapenems, e.g. meropenem ```
37
Start Smart
do not start antimicrobial therapy unless there is clear evidence of infection take a thorough drug allergy history initiate prompt effective antibiotic treatment within one hour of diagnosis (or as soon as possible) in patients with severe sepsis or life-threatening infections. Avoid inappropriate use of broad-spectrum antibiotics comply with local antimicrobial prescribing guidance document clinical indication (and disease severity if appropriate), drug name, dose and route on drug chart and in clinical notes* include review/stop date or duration obtain cultures prior to commencing therapy where possible (but do not delay therapy) prescribe single dose antibiotics for surgical prophylaxis where antibiotics have been shown to be effective document the exact indication on the drug chart (rather than stating long term prophylaxis) for clinical prophylaxis
38
Then Focus
reviewing the clinical diagnosis and the continuing need for antibiotics at 48*-72 hours and documenting a clear plan of action - the ‘antimicrobial prescribing decision’ the five ‘antimicrobial prescribing decision’ options are: 1. Stop antibiotics if there is no evidence of infection 2. Switch antibiotics from intravenous to oral 3. Change antibiotics – ideally to a narrower spectrum – or broader if required 4. Continue and document next review date or stop date 5. Outpatient Parenteral Antibiotic Therapy (OPAT) it is essential that the review and subsequent decision is clearly documented in the clinical notes and on the drug chart where possible eg stop antibiotic