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
beta lactams "rules"
- 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
26
the different beta lactam antibiotics differ by ...
the structures that are linked to b-lactam ring
27
glycopeptides rules
- 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
28
aminoglycosides rules
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)
29
tetracyclines rules
broad spectrum, toxic - GN and GP - toxic toward developing teeth and bones - NOT for children
30
macrolides rules
GP only; erythromycin commonly tested - tested for GP only (erythromycin) - may be used for some 'special' GN like Neisseria, Bordetella, Chlamydia
31
lincosamide rules
- 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
antibiotic associated with C. diff
lincosamide (clindamycin)
33
quinolones rules
wide rang of aerobic and facultative anaerobes - includes fluoroquinolones (cipro, levofloxacin, etc.) - affects DNA replication - can be taken orally - concentrates well in urine
34
sulfonamides/SXT
- 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
VRE drug
linezolid
36
MRSA gene
MecA codes for PBP change (PBP2A and PBP2A')
37
MRSA test
cefox disc may require oxacillin Etest if vitek MIC is low
38
T or F. When screening for MRSA, patients not treated
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
why is cefoxitin used to ID clox resistance?
better inducer of MecA resistance than oxacillin or other
40
hetero population is common with this
MRSA can make ID difficult some colonies S and some R incubating cefox testing at 35C can help enhance MecA resistance
41
VRE gene
VanA and VanB (passed on by plasmids; not VanC though!) alteration of vancomycin binding site
42
VRE screening
rectal on VRE chromagar
43
VRE clinical
any site; urine most common
44
VRE clinical
any site; urine most common
45
how to test for VRE
Vancomycin Etest for confirmation
46
highest MIC
256 ug/mL
47
VISA/VRSA
VISA = thickening of cell wall VRSA = VanA from VRE (keep MRSA and VRE patients away)
48
why do we carefully monitor Vancomycin results on MRSA
in case of VRSA emergencw
49
how to test for VISA/VRSA
vanc E test to confim MIC as automated susceptibility testing does not accurately pick up resistance in Staph
50
beta-lactamase
- 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
b lactamase class 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
drug of choice for H. influenzae
ampicillin but if BLP ... can't use it so we don't even test amp for BLP H. influenza
53
clavulanic acid
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
ESBL
- 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
ESBL disc test... why not nitrocefin?
this is not constitutive, it's inducible!! must be growing in presence of 3rd gen to produce enzyme
56
EXBL disc test
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
MBL
- 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
screening for MBL
chromagar (CRE) used sparingly when requested
59
any site resistant to 3d gen cephalosporin and carbapenem
require further testing MBL??
60
how to test for MBL
MAST discs; b lactamase inhibitor has no use here
61
KESC group
Klebsiella, Enterobacter, Serratia, Citrobacter
62
KESC group
Klebsiella, Enterobacter, Serratia, Citrobacter
63
MBL ID
double disc test - one disc with mero - one disc with mero + MBL inhibitor (dipicolinic acid or DPA) if zon > or = 5mm = MBL!
64
DPA
MBL inhibitor; helps with ID
65
GNB with carbapenem reisstance, which is only antibiotic sens
colistin
66
colistin resistance
- MCR-1 mobilized colistin resistance - modified target site - plasmid-mediated so IC Concern - Enterobacteriaceae often from livestock/food animals
67
how to identify colistin resistance
PCR to ID MCR-1 gene
68
intrinsically resistance to colistin
PMP group and Serratia = does not need further ID of MC-1
69
ICR
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
ICR organisms
S. aureus, B-hem Strep, anaerobic GPC
71
how to test ICR
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
D test
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