Antimicrobial resistance Flashcards
2 broad categories for resistance
- Intrinsic resistance: natural & inherited
2. Acquired resistance: Successful genetic mutation
Causes of Antimicrobial resistance (slide 4)
- over prescribing
- patients not finishing treatment
- antibiotics in farming
- poor infection control in healthcare
- lack of hygiene & poor sanitisation
- Lack of antimicrobial discovered
antibiotic creed (mindme)
Microbiology guide (if possible) Indications should be EVIDENCE based Narrowest spectrum (SPECIFIC) DOSAGE appropriate to site of infection Minimise DURATION of therapy Ensure mono therapy (one drug effective to kill multiple infections)
What mediates AMPC B-lactamases? chromosome or plasmid? & what’s the expression?
Either:
- chromosome: inducible expression
- Plasmid: constitutive expression
Name three of the five mechanisms of antibiotic resistance used by bacteria?
- Alter targert/receptor molecule =less binding
- Alter membrane so there’s no way drugs can bind to
- Produce alternative enzymes OR use diff. pathway: e.g. alternative for producing folic acid
- Inactivation of drug: degrade or modify drug
- Drug actively pumped out of cell
List the names of the five chemical B-lactamase inhibitors that can be incorporated into antibacterial drugs.
Clavulanic acid Tazobactam Sulbactam Avibactam Vaborbactam
What are extended spectrum B-lactamases (ESBL)?
ESBL are enzymes that encode resistance to penicillins, cephalosporins (1GC, 2GC, 3GC, 4GC) and atreonam.
* Encoded on a plasmid
2 signs you have an ESBL on a susceptibility plate
- reduced susceptibility to aztreonam (ATM) or ESB-lactams (3GC) > R to strong broad spec.
- Keyhole effect when AMC (w/ clauv. acid) in b/w 2 B-lactams inhibitor (e.g. CTX & ATM) > inhibits B-lactamases
What is the difference between the ESBL and the AMPC encoded enzymes in terms of the antimicrobial agents that each inhibit? MORE?
- AMPC: R to all B-lactams (penicillins, 1-3GC) & most inhibitors (EXCEPT 4GC & aztreonam)
- ESBL R extended spectrum (3GC, 4GC) B-lactams. BUT inhibitors work
What antimicrobial agents do the (metallo B-lact) NDM-1 enzymes inhibit? What current treatment option exist for each?
R to IPM & meropenam (MPM) = carbapenams.
Treatment: Aztreonam(ATZ), Colistin, tigecycline, EDTA? (bc chelate Zn)
What is empirical antibiotic therapy?
antibiotics given before ID the organism causing the infection
Which organisms are generally associated with the production of inducible AMPC B-lactamases? (ESCHAPpM)
- Enterobacter (E. cloacae)
- Serratia marcescens
- Cirtobacter freundii
- Hafnei alvei
- Aeromonas (all except A.sobria, A. veronii)
- Providencia
- proteus (*sometimes)
- Morganella morganii
How can you tell if an inducible AMPC enzyme is being produced in the lab? 5 points (Could you draw the profile?)
- resistance to AMC (Augmentin) - not inhibited by clauvanic acid (B-lactamase inhibitor)
- R to multiple disks
- S to 3GC (e.g. CTX)
- ?* Imipenim (IPM) induce visible R (enhanced growth) to cephalosporines b/w it
- Sensitive to 4GC (e.g. CPO/cefpirome, FEP/cefepime)
How can a plasmid mediated AMP C be detected in lab?
- PM AMPC inhibited by atreonam & boronic acid
- Resistant to AMC (augmentin)
- Susceptible to cefepime FEP (4GC)
In disc susceptibility tests, why is it important to place an AMC disc adjacent to a 3GC?
- Augmentin is amoxillin + clavulanic acid (inhibitor)
- 3GC (e.g. CTX)
- If microbe R to 3GC but microbe is S w/ AMC = inhibitor works = keyhole = ESBL
