Antimicrobials in clinical practice Flashcards
Dental abscess antibiotics
Amoxicillin 500mg tds x 5/7
Or
Penicillin V 500mg qds x 5/7
Considerations when giving antibiotics
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?
Are antibiotics necessary?
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?
Dental abscess - primary management
pulpectomy / incision and drainage
analgesia
The addition of antibiotics is not recommended for a localized dental abscess.
Dental abscess- antibiotics indicated if
No possibility of immediate attention by a dental practitioner,
Or
Features of severity / increased risk …
Features of severity or increased risk
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.
Is it a dental abscess? **
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
Dental abscess - differential diagnosis
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
What is the site of infection?
What organisms should be covered?
Which antibiotics will penetrate that site?
Pharyngitis vs dental abscess
Pharyngitis: Streptococcus pyogenes EBV Dental abscess: Viridans group streptococci Anaerobes Gram negative rods
Bacteria associated with dental infection
Bacteroides Fusobacterium Actinomyces Peptostrep P. melaninogenica S. viridans S. aureus Haemophiius T. spp. (know gram and an/aero)
Antimicrobials and oral infections: penicillin
S. sanguis (viridans)
N. gonnorhoeae
T. spp.
Anaerobes +/-
Antimicrobials and oral infections: Flucloxacillin
S. aureus
Antimicrobials and oral infections: Ampicillin
S sanguis (viridans) N. gonnorhoeae H. influenzae (+/-) T. spp Anaerobes +/-
Antimicrobials and oral infections: Cefuroxime
S sanguis (viridans) S. aureus (+/-) N. gonnorhoeae H. influenzae T. spp Anaerobes +/-
Antimicrobials and oral infections: clindamycin
S sanguis (viridans)
S. aureus
Anaerobes
Antimicrobials and oral infections: erythromycin (macrolides)
S sanguis (viridans)
S. aureus (+/-)
H. influenzae (+/-)
Antimicrobials and oral infections: Gentamicin
S sanguis (viridans) S. aureus (+/-) N. gonnorhoeae H. influenzae T. spp.
Antimicrobials and oral infections: metronidazole
Anaerobes ++
Primary and acquired resistance
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
How do bacteria resist antibiotics?
Change antibiotic target
Destroy antibiotic
Prevent antibiotic access
Remove antibiotic from bacteria
How does resistance develop?
Intrinsic - naturally resistant
Acquired
-spontaneous gene mutation
-horizontal gene transfer –> conjugation, transduction, transformation
How do we detect resistance/ sensitivity?
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
Antibiotic sensitivity testing
Dilutional liquid culture MIC and MBC
Antibiotic discs
E-tests
Breakpoint plates
plates with a specific ‘breakpoint’ concentration of antibiotic in and see if a given inoculum grows or not
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
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
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)
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
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.
Two major determinants of bacteria killing include
concentration and the time that the antibiotic remains on these binding sites
Concentration-dependent killing
Key parameter is how high the concentration is above MIC
Peak conc / MIC ratio
-aminoglycosides
-quinolones
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),
What is the appropriate or available route of administration?
And dosage interval/ duration
e.g. Strep pharyngitis: Penicillin V, oral, 6 hourly, 10 days
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)
Risk of C. difficile
5 Cs Ciprofloxacin Clindamycin Cephalosporins Co-amoxiclav (augmentin) Carbapenems, e.g. meropenem
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
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
