Anti-microbial resistance Flashcards
(28 cards)
what is the mech of MRSA antibiotic resistance?
Resistance to methacillin caused by changes to cell wall structure
- PBP2a is a penicillin binding protein (76 kda), mediated by mecA gene.
- Penicillins and cephalosporins cannot bind to PBP2a
- Results in resistance to all penicillin class agents and
cephalosporins - MecA is carried on a mobile genetic element called Staphylococcal Cassette Chromosome mec ( SCC mec)
there are 5 mec variants, including things like “UK MRSA” which also encodes for cipro resistance
how do we orally treat MRSA (classically)
rifampicin and fusidic acid
clindamycin is useful for CA-MRSA
what is the difference between vanA and vanB in VRE?
Van A is:
resistant to vanco
resistant to teicoplanin
Van B is:
resistant to vanco
sens to teicoplanin
what is the mechanism of gram neg penicillin resistance?
typically this is the whole beta lactam production
what are some of the subtypes of carbapenemases?
what are the important subtypes within that classification?
they are either serine beta-lactamases or metallo-beta-lactamases
There is a specific high interest one called NDM “New Dehli Metallobetalactamase”
this one is srs business
true or false:
vancomycin resistance in S. aureus is associated with an abnormally thick cell wall?
true. true for staph aureus, but not for VRE
in VRE is it plasmid or transposon derived alteration of the binding site
meningitis
CSF: lots of neutros and gram pos diplococci
what do we give?
this is likely to be pneumococcus
there is ~10% pen-resistance in the community.
give vanc and a 3rd gen cephalosporin (cefotaxime or CTX)
How does pneumococcus get penicillin resistance?
altered PBP
beta-lactamase is usually gram neg
ribosomal inhibition of protein synthesis is gram neg and TB
transposon mediated resistance is seen in Staph
q. how does enterococci get vanc resistance?
a. change in the cell wall to prevent vanco binding
q. what is the treatment for enterococcus faecalis bloodstream infection?
linezolid
what sort of meningitis does leptospira cause?
typically an aseptic meningitis treated by ben pen or 3rd gen ceph
what is the most common mechanism of Gram positive organisms having resistance to penicillin?
apparently it is beta lactamase production, and this out ranks the PBP modification
what is the predominant enterococcal sp involved in non-VRE infection?
what about VRE?
Non-VRE: E. faecalis
VRE: E. faecium
what is the difference in VanA versus VanB with respect to antibiotic choices?
VanA is a more worrying phenotype, because it is also resistant to teicoplanin
VanB is vanc resistant, but teicoplanin sensitive
what are our treatment options for Acinetobacter baumannii?
this bad boy has pretty significant resistances. it used to be carbapenem sensitive, but this has now changed.
First line would be amikacin (an aminoglycaside)
second line teicoplanin
what is the important thing about Stenotrophomonas maltophilia, with respect to infection control?
this is another of our nasty gram negatives.
this one is intrinsically resistant to carbapenems
drug of choice is bactrim
what is especially bad news about the C. difficle ribotype 027 and 078?
also, what do the c diff exotoxins do?
these are highly toxigenic strains.
they have only recently emerged out of Canada.
They produce 20x greater toxin and an additional binary toxin
they are especially associated with fluoroquinolone treatment
by the way, the exotoxins bind to the intestingal epithelial cell receptors and induce fluid secretion and acute inflammatory infiltrate
what is the most common aetiological agent causing hospital acquired pneumonia?
aerobic gram negative bacilli
this is typically after the first 48 hours (during which time it is the normal community pathogens)
how do we determine if a patient’s VRE colonisation came from another particular patient?
we use a technique called pulse-field gel electrophoresis
in this, we cut up the genome and PCR it, then compare the DNA
someone presents after 24 hours after exposure to confirmed measles. They had significant exposure
what would you do for treatment?
within 72 hours of exposure, you could give the measles live attenuated vaccine (unless there was contraindications)
after that time, you should give normal immunoglobulin
how does the PVL (Panton-Valentine Leucocidin) toxin producing staph present?
pyogenic skin infections. Lots of them.
what is a common side effect to prolonged Linezolid use?
thrombocytopenia
which antibiotic can exacerbate myaesthenia gravis?
any of the aminoglycosides, particularly gentamicin
How does pneumococcus get penicillin resistance?
altered PBP
beta-lactamase is usually gram neg
ribosomal inhibition of protein synthesis is gram neg and TB
transposon mediated resistance is seen in Staph
