Anti-microbial resistance

Question 1

what is the mech of MRSA antibiotic resistance?

Answer 1

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

Question 2

how do we orally treat MRSA (classically)

Answer 2

rifampicin and fusidic acid

clindamycin is useful for CA-MRSA

Question 3

what is the difference between vanA and vanB in VRE?

Answer 3

Van A is:
resistant to vanco
resistant to teicoplanin

Van B is:
resistant to vanco
sens to teicoplanin

Question 4

what is the mechanism of gram neg penicillin resistance?

Answer 4

typically this is the whole beta lactam production

Question 5

what are some of the subtypes of carbapenemases?

what are the important subtypes within that classification?

Answer 5

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

Question 6

true or false:

vancomycin resistance in S. aureus is associated with an abnormally thick cell wall?

Answer 6

true. true for staph aureus, but not for VRE

in VRE is it plasmid or transposon derived alteration of the binding site

Question 7

meningitis
CSF: lots of neutros and gram pos diplococci

what do we give?

Answer 7

this is likely to be pneumococcus

there is ~10% pen-resistance in the community.

give vanc and a 3rd gen cephalosporin (cefotaxime or CTX)

Question 8

How does pneumococcus get penicillin resistance?

Answer 8

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

Question 9

q. how does enterococci get vanc resistance?

Answer 9

a. change in the cell wall to prevent vanco binding

Question 10

q. what is the treatment for enterococcus faecalis bloodstream infection?

Answer 10

linezolid

Question 11

what sort of meningitis does leptospira cause?

Answer 11

typically an aseptic meningitis treated by ben pen or 3rd gen ceph

Question 12

what is the most common mechanism of Gram positive organisms having resistance to penicillin?

Answer 12

apparently it is beta lactamase production, and this out ranks the PBP modification

Question 13

what is the predominant enterococcal sp involved in non-VRE infection?

what about VRE?

Answer 13

Non-VRE: E. faecalis

VRE: E. faecium

Question 14

what is the difference in VanA versus VanB with respect to antibiotic choices?

Answer 14

VanA is a more worrying phenotype, because it is also resistant to teicoplanin

VanB is vanc resistant, but teicoplanin sensitive

Question 15

what are our treatment options for Acinetobacter baumannii?

Answer 15

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

Question 16

what is the important thing about Stenotrophomonas maltophilia, with respect to infection control?

Answer 16

this is another of our nasty gram negatives.

this one is intrinsically resistant to carbapenems

drug of choice is bactrim

Question 17

what is especially bad news about the C. difficle ribotype 027 and 078?

also, what do the c diff exotoxins do?

Answer 17

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

Question 18

what is the most common aetiological agent causing hospital acquired pneumonia?

Answer 18

aerobic gram negative bacilli

this is typically after the first 48 hours (during which time it is the normal community pathogens)

Question 19

how do we determine if a patient’s VRE colonisation came from another particular patient?

Answer 19

we use a technique called pulse-field gel electrophoresis

in this, we cut up the genome and PCR it, then compare the DNA

Question 20

someone presents after 24 hours after exposure to confirmed measles. They had significant exposure

what would you do for treatment?

Answer 20

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

Question 21

how does the PVL (Panton-Valentine Leucocidin) toxin producing staph present?

Answer 21

pyogenic skin infections. Lots of them.

Question 22

what is a common side effect to prolonged Linezolid use?

Answer 22

thrombocytopenia

Question 23

which antibiotic can exacerbate myaesthenia gravis?

Answer 23

any of the aminoglycosides, particularly gentamicin

Question 24

How does pneumococcus get penicillin resistance?

Answer 24

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

Question 25

how does enterococci get vanc resistance?

Answer 25

a. change in the cell wall to prevent vanco binding

Question 26

q. what is the treatment for enterococcus faecalis bloodstream infection?

Answer 26

linezolid

Question 27

what sort of meningitis does leptospira cause?

Answer 27

typically an aseptic meningitis treated by ben pen or 3rd gen ceph

Question 28

what is the most common mechanism of Gram positive organisms having resistance to penicillin?

Answer 28

apparently it is beta lactamase production, and this out ranks the PBP modification