Flashcards in Antimicrobial resistance Deck (19)
2 broad categories for resistance
1. 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)
AMPC B-lactamases chromosome or plasmid* (not done double cehck)
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.
importnat B-lactamase profiles
-Penicillinase: TEM1, TEM2, SHV1
-AMPC on chromo.
-AMPC on plasmid
-non-AMPC inducible cephalosporinase
What are extended spectrum B-lactamases (ESBL)?
ESBL are enzymes that encode resistance to penicillins, cephalosporins (1GC, 2GC, 3GC, 4GC) and atreonam
How are they detected in a clinical laboratory (describe at least three methods i.e. don’t just list them off. How do they work)?
1. reduced susceptibilit to atreozam or ESB-lactams (3GC)
2. Keyhole effect when inhibitor inhibits resistance (of growth): inhibitor (e.g. AMP) in b/w B-lactams
What is the difference between the ESBL and the AMPC encoded enzymes in terms of the antimicrobial agents that each inhibit? *MORE?*
-AMPC inhibit cephalosporinase (Type 1 or Class C)
-ESBL inhibit extended spectrum (3GC, 4GC) B-lactams
What antimicrobial agents do the NDM-1 and KPC enzymes inhibit? What current treatment option exist for each? *NOTE DONE
-NDM-1: inhibit beta lactams. Treatment: *
- KPC: inhibit carbapenams. treatment: colistin & tigecycline
What is empirical antibiotic therapy?
Which organisms are generally associated with the production of inducible AMPC B-lactamases?*(not sure)
- E. coli
- K. pneumoniea
- Salmonella sp
How can you tell if an inducible AMPC enzyme is being produced? Could you draw the profile?
1. resistance to AMC (Augmentin) - not inhibited by clauvanic acid (B-lactamase inhibitor)
2. S to 3GC (e.g. CTX)
3. Imipenim (IPM) induce visible resistance (enhanced growth) to cephalosporines b/w it
4. Sensitive to 4GC
5. multiple resistant to most discs
How can a plasmid mediated AMP C be detected?
- 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 (CTX)
- If microbe R to 3GC but microbe is S w/ AMC = inhibitor works = keyhole = ESBL
List two possible clinical consequences (to the patient) of prolonged, broad-spectrum antibiotic use? *
- introduce selective pressure in NF = mutate = resistant to anti-b
Can you recognise the presence of an ESBL, an inducible AMPC, and an inducible non-AMP C by looking at a susceptibility profiles?
- AMPC = R to cephalosporinase + S to inhibitor (like clavunic acid)
- non-AMP C = R to cephalosporinase + R inhibitor (like AMP C)