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MLSCI 340 > LAB 15 -Antimicrobials > Flashcards

LAB 15 -Antimicrobials Flashcards

1
Q

CLSI warnings - the following combos may appear active in vitro but are not effective clinically and should NOT be reported as susceptible

A

Salmonella, Shigella sp = 1st and 2nd gen cephalosporins, cephamycins, and aminoglycosides

oxacillin-resistant Staph sp. = penicillins, b lactam/ b lactamase inhibitor combinations, anti-staphylococcal cephems, and carbapenems

Enterococcus sp = aminoglycosides (except high concentrations), cephalosporins, clindamycin, and SXT

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2
Q

amikacin

A

aminoglycoside

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3
Q

vancomycin

A

glycopeptides

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4
Q

naladixic acid

A

quinolones

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5
Q

erythromycin

A

macrolides
(only GP)

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6
Q

cefuroxime

A

cephalosporins

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7
Q

Ciprofloxacin

A

quinolones

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8
Q

Meropenem

A

Carbapenems

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9
Q

Co-trimoxazole

A

sulfonamides

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10
Q

cephalothin

A

cephalossporin

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11
Q

gentamicin

A

aminogycside

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12
Q

tobramycin

A

aminoglycoside

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13
Q

ampicillin

A

penicillins

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14
Q

clindamycin

A

lincosamides

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15
Q

imipenem

A

carbapenem

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16
Q

cell wall synthesis antimicrobials

A

beta lactams
vancomycin

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17
Q

protein synthesis antimicrobials

A

aminoglycosides
tetracylines
chloramphenicol
macrolides
lincosamides
oxazolidinones
streptogramins

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18
Q

DNA and RNA synthesis antimicrobials

A

fluoroquinolones
rifamycins (RNA)
metronidazole (DNA)

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19
Q

metabolic pathways antimicrobials

A

sulfonamides
trimethoprim
nitrofurantoin

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20
Q

cell membrane and integrity antimicrobials

A

polymyxin B
Colistin
Daptomycin

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21
Q

beta-lactams

A

bind th enzyme inhibiting transpeptidation and inhibit cell wall synthesis (interferes with peptidoglycan cross-linking

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22
Q

vancomycin

A
  • a glycopeptide
  • bind the end of the peptidoglycan interfering with transpeptidation, inhibition of cell wall synthesis and growth
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23
Q

how do sulfonamides and trimethoprim work together?

A

inhibit folic acid production at two different spots on the pathway

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24
Q

how does Nitrofurantoin inhibit metabolic pathways?

A

it binds to ribosomal proteins and rRNA to affect the folic acid pathway

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25
Q

beta lactams “rules”

A
  • penicillins = BLNGP and GNDC; unable to penetrate outer mem of most gnb
  • cephalosporins = diff generations have diff spectrums
  • carbapenems = very broad spectrum to cover many GP and GN organisms
  • monobactams = effective against GN other than strict anaerobes
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26
Q

the different beta lactam antibiotics differ by …

A

the structures that are linked to b-lactam ring

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27
Q

glycopeptides rules

A
  • aeorbic GP
  • similar to BLs
  • since targeting cell wall through peptidoglycan, no human toxicity
  • do not pass into CSF, cannot be taken orally
  • saved for serious infections
  • GN resistant bc OM is impermeable to large size of molecules
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28
Q

aminoglycosides rules

A

mostly aerobic and facultative GNB
transported into bacteria using oxidative metabolism so cant use with anaerobes or organisms that can only metabolize fermentatively (NO STREP)

  • Enterobacteriaecea and P. aeruginosa
  • serious infections with GP organisms but will be paired with another drug
  • Enterococcus at high concentration (Gent Synergy)
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29
Q

tetracyclines rules

A

broad spectrum, toxic
- GN and GP
- toxic toward developing teeth and bones
- NOT for children

30
Q

macrolides rules

A

GP only; erythromycin commonly tested
- tested for GP only (erythromycin)
- may be used for some ‘special’ GN like Neisseria, Bordetella, Chlamydia

31
Q

lincosamide rules

A
  • clindamycin = similar to eryhtro + GN anaerobes
  • often used if anaerobe infection/co-infection
  • associated with C.diff infection due to activity against GN anaerobes so clear out large amounts of gut flora
32
Q

antibiotic associated with C. diff

A

lincosamide
(clindamycin)

33
Q

quinolones rules

A

wide rang of aerobic and facultative anaerobes
- includes fluoroquinolones (cipro, levofloxacin, etc.)
- affects DNA replication
- can be taken orally
- concentrates well in urine

34
Q

sulfonamides/SXT

A
  • work at different points of folate pathway; often paired for better killing power
  • toxicity not a concern bc we ingest folate
  • common for UTIs as it concentrates in urine
  • can be taken orally
35
Q

VRE drug

A

linezolid

36
Q

MRSA gene

A

MecA codes for PBP change (PBP2A and PBP2A’)

37
Q

MRSA test

A

cefox disc
may require oxacillin Etest if vitek MIC is low

38
Q

T or F. When screening for MRSA, patients not treated

A

T!
nose and groin to chromagar
just a carrier; not causing infection
positive pts put under precautions by infection control so doesn’t spread

39
Q

why is cefoxitin used to ID clox resistance?

A

better inducer of MecA resistance than oxacillin or other

40
Q

hetero population is common with this

A

MRSA
can make ID difficult
some colonies S and some R
incubating cefox testing at 35C can help enhance MecA resistance

41
Q

VRE gene

A

VanA and VanB (passed on by plasmids; not VanC though!)
alteration of vancomycin binding site

42
Q

VRE screening

A

rectal on VRE chromagar

43
Q

VRE clinical

A

any site; urine most common

44
Q

VRE clinical

A

any site; urine most common

45
Q

how to test for VRE

A

Vancomycin Etest for confirmation

46
Q

highest MIC

A

256 ug/mL

47
Q

VISA/VRSA

A

VISA = thickening of cell wall
VRSA = VanA from VRE (keep MRSA and VRE patients away)

48
Q

why do we carefully monitor Vancomycin results on MRSA

A

in case of VRSA emergencw

49
Q

how to test for VISA/VRSA

A

vanc E test to confim MIC as automated susceptibility testing does not accurately pick up resistance in Staph

50
Q

beta-lactamase

A
  • H. influenzae resistant to ampicillin
  • class A - basic penicillinase (TEM-1)
  • enzyme that hydrolyzes balctam ring
  • Haemophilus, Neisseria, M. catarhalis, B. fragilis
  • cefinase or nitrocefin as constitutive enzyme
51
Q

b lactamase class A

A

basic and weak
only R to amp, amox, penicillin
other penicillins (clox, ox, meth) not affected
NOTE: why we treat clox for S. aureus bc usually BLP

52
Q

drug of choice for H. influenzae

A

ampicillin
but if BLP … can’t use it so we don’t even test amp for BLP H. influenza

53
Q

clavulanic acid

A

beta lactamase inhibitor; ‘suicide inhibitor’
- substrate so enzyme is used up.. leaving antimicrobial to be effective against the organism
- AMOX (AMC) is tested with clavulanate; BLP amp will be reported as R so test AMC instead

54
Q

ESBL

A
  • E. coli R to 3rd gen cephalosporins
  • class A - basic penicilllinase
  • extended-spectrum = effective on more rings
  • plasmid-mediated = IC concern
  • ESBL disc test
  • concern in Enterobacteriaceae
  • we don’t screen but if any 3rd gen cephalosporin comes up R, then testing required
55
Q

ESBL disc test… why not nitrocefin?

A

this is not constitutive, it’s inducible!! must be growing in presence of 3rd gen to produce enzyme

56
Q

EXBL disc test

A

paired discs used
one disc has 3rd gen cephalosporin (Cepofoxime, Cefotaxime, Ceftazidime)
AND a 3rd gen cephalosporin with clavulanic acid
5mm diff between two discs

57
Q

MBL

A
  • class B - requies zinc for action; ‘metallo’
  • found in GNB - Enterobacteriaceae, P. aeruginosa, Acinetobacter
  • R to all b-lactams including carbapenems
  • three main types = VIM, IMP, NDM
58
Q

screening for MBL

A

chromagar (CRE) used sparingly when requested

59
Q

any site resistant to 3d gen cephalosporin and carbapenem

A

require further testing
MBL??

60
Q

how to test for MBL

A

MAST discs; b lactamase inhibitor has no use here

61
Q

KESC group

A

Klebsiella, Enterobacter, Serratia, Citrobacter

62
Q

KESC group

A

Klebsiella, Enterobacter, Serratia, Citrobacter

63
Q

MBL ID

A

double disc test
- one disc with mero
- one disc with mero + MBL inhibitor (dipicolinic acid or DPA)
if zon > or = 5mm = MBL!

64
Q

DPA

A

MBL inhibitor; helps with ID

65
Q

GNB with carbapenem reisstance, which is only antibiotic sens

A

colistin

66
Q

colistin resistance

A
  • MCR-1 mobilized colistin resistance
  • modified target site
  • plasmid-mediated so IC Concern
  • Enterobacteriaceae often from livestock/food animals
67
Q

how to identify colistin resistance

A

PCR to ID MCR-1 gene

68
Q

intrinsically resistance to colistin

A

PMP group and Serratia = does not need further ID of MC-1

69
Q

ICR

A

inducible clindamycin resistance
- some S. aureus resistant to clinda, not all inducible
- erm gene = constitutive and inducible resistance
- may test sens in vitro but treatment fails in vivo

70
Q

ICR organisms

A

S. aureus, B-hem Strep, anaerobic GPC

71
Q

how to test ICR

A

if Erythromycin I/R and Clinda = S = further testing necessary =Double Disc test or D test (2 discs specific distance and incubated overnight)

  • if flattening = resistance induced; clinda R
  • if circular zone = negative = clinda S
72
Q

D test

A

used to identify inducible resistance but does not mean pt has to b on both antibiotics for clinda to be R
organism will quickly demonstrate resistance in patient when exposed to clinda for treatment alone

MLSCI 340 (16 decks)

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