Antibiotics/Resistance Flashcards

1
Q

Aminoglycoside concerns

A

Ear and kidney toxicity

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2
Q

Aminoglycoside mechanism

A

Aminoglycosides bind irreversibly to bacteria 30S and 50S ribosomal subunits to prevent initiation complex formation + protein synthesis BacterioCIDAL

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3
Q

Aminoglycoside spectrum

A

Primarily effective against GRAM NEGATIVES but synergistic with beta-lactams for G+

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4
Q

2 drugs commonly used for anaerobes

A

Metranidazole or clindamycin

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5
Q

Nucleic acid synthesis inhibitor used for cryptococcus meningitis

A

5-FC

Bone marrow toxicity and resistance can develop in days so always use in combination

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6
Q

Antifungal with ability to form pore in cell wall

A

Amphotericin B

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7
Q

Azole mechanism

A

Inhibition of cytochrome P-450 to block synthesis of ergosterol

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8
Q

Echinocandins do not work on…

A

Zygomycetes

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9
Q

Target of echinocandins

A

Block B-1,3-glucan synthase inhibitors

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10
Q

Good drug for mycoplasma (no cell wall)

A

Azithromycin (Macrolide)

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11
Q

Classes of beta-lactams

A
  1. Penicillins 2. Cephalosporins 3. Monobactams 4. Carbapenems
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12
Q

Common concern for treating patients with beta-lactams

A

Allergies (mild to anaphylaxis)

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13
Q

Beta-lactam mechanism

A

inhibits cell wall synthesis by binding to and preventing PBP function of cross-linking NAM and NAG BacterioCIDAL

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14
Q

Ceftriaxone is what generation cephalosporin?

A

3rd

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15
Q

Cefezolin is what generation cephalosporin?

A

1st often used as surgical prophylaxis

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16
Q

Subclasses of cephalosporins

A
  1. Classified from 1st to 5th generation 1st narrow spectrum (G+) 5th broad spectrum and better with G-
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17
Q

Clindamycin limitations

A

Poor penetration into CSF –> don’t use for meningitis

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18
Q

Clindamycin mechanism

A

Bind 50S ribosomal subunit, prevents elongation of peptide chains—suppresses protein synthesis (same spot as macrolides) Can be bacteriostatic or bacteriocidal

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19
Q

Fluoroquinalone spectrum with increasing generation

A

Early better for G- Later better for G+

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20
Q

First gen fluoroquinalone

A

Nalidixic acid

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21
Q

Third gen fluoroquinalone

A

tosufloxacin

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22
Q

Second gen fluoroquinalones

A

Ciprofloxacin and levofloxacin

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23
Q

Fourth gen fluoroquinalones

A

Moxifloxacin and Gemifloxacin

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24
Q

Fluoroquinolone mechanism

A

Inhibit DNA gyrase +/- topoisomerase IV to inhibit chromosomal replication BacterioCIDAL

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25
Q

Leuconostoc has intrinsic resistance to what antibiotic

A

Vancomycin

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26
Q

Klebsiella isolate resistant to aztreonam and ceftriaxone has what resistance mechanism?

A

K-1 beta lactamase

27
Q

Macrolide side effects

A

GI distress

28
Q

Macrolide spectrum

A

Broad-spectrum: Gram positives, some Gram-negative, anaerobes, atypical mycobacteria, and “atypical” respiratory pathogens (mycoplasma, chlamydiae, Legionella) that are less susceptible to β-lactams

29
Q

Macrolides mechanism

A

Bind reversibly to 23S of rRNA of the 50S ribosomal subunit, block translocation of tRNA from acceptor to donor side on ribosome BacterioSTATIC

30
Q

A predefined stable antibiotic gradient is present on a thin carrier strip.

A

E-test

31
Q

A paper disk with defined amount of antibiotic is used to generate a dynamically changing gradient of antibiotic concentrations in the agar in the vicinity of the disk. ZOI gives qualitative indication if whether the bug is susceptible.

A

Kirby-Bauer Method

32
Q

the lowest concentration of an antimicrobial that will kill an organism.

A

MBC = Minimum Bactericidal Concentration

33
Q

What density should the inoculum for Kirby-Baur tests be?

A
  1. 5 McFarland
  2. 5 x 108 organisms/mL
34
Q

the lowest concentration of an antimicrobial that will inhibit the visible growth of a microorganism after overnight incubation.

A

MIC = Minimum inhibitory concentration

35
Q

Metronidazole coverage

A

Requires reduction of nitro group under anaerobic conditions, therefore only effective against anaerobes and protozoa

36
Q

Metronidazole mechanism

A

Causes breaks in DNA

37
Q

Beta-lactam resistant to β-lactamases. Purely Gram-negative coverage, primarily active against members of the family Enterobacteriaceae

A

Monobactams

38
Q

Polymixin concerns

A

Kidney and neurotoxicity

39
Q

Polymixin uses

A

Primarily for multi-drug resistant Gram negatives (eg. Pseudomonas) Also used as a topical Ab with no toxicity concerns

40
Q

Polymixins mechanism

A

Large polypeptides with cationic detergent effect that disrupts cell membrane

41
Q

AmpC characteristics

A

Not inhibited by bet-lactamase inhibitors

42
Q

AmpC mechanism

A

Cascade triggered by the sensing of damage to the cell wall. Induces AmpC expression, a beta-lactamase

43
Q

Name the SPICEM organisms and what resistance patten they can carry

A

SPICEM organisms are members of the Enterobacteriaceae that often carry an inducible AmpC gene

  • Serratia
  • Providencia
  • Indole-positive Proteus (vulgaris)
  • Citrobacter
  • Enterobacter
  • Morganella
44
Q

Transferrable carbapenemase

A

KPC

45
Q

Carbapenemase detection

A

Hydrolysis of immipenem Modified Hodge test- test isolate produces the enzyme and allows growth of a carbapenem susceptible strain towards a carbapenem disk

46
Q

Resistance to carbapenems caused by…

A

Efflux or carbapenemase

47
Q

Erythromycin and Clindamycin resistance mechanism

A

Methylation of 50S ribosome

48
Q

Erythromycin/Clindamycin resistance detection

A

D-zone test

49
Q

ESBL characteristics

A

Sensitive to beta-lactamases

50
Q

General mechanisms of antimicrobial resistance

A

Efflux pumps Restricted access to target Target modification Inactivating enzymes

51
Q

Mechanism of MRSA

A

mecA gene encodes an altered penicillin-binding-protein, PBP2a, that beta-lactams cannot bind to. Often on a mobile element, SCCmec, so there are concerns for spread of resistance

52
Q

What drug do we use to look for MRSA?

A

Cefoxitin

Historically, oxicillin has been used but cefoxitin is more stable and better able to induce the mecA gene

53
Q

VISA mechanism

A

Cell wall thickening traps vancomycin from penetrating to deeper layers of peptidoglycan

54
Q

VRE mechanism

A

VanA and VanB alter terminal end of D-ala so that vancomycin can no longer bind

55
Q

Species of Enterococcus most likely to be VRE

A

E. faecium Treat with daptomycin instead

56
Q

Rifampin mechanism

A

Inhibits bacterial DNA-dependent RNA polymerase -> inhibits transcription

57
Q

Rifampin resistance mechanism

A

point mutations in rpoB occur quickly Always must be prescribed in combination

58
Q

Sulfas/trimethoprim mechanism

A

inhibit folate synthesis, thereby inhibiting purine metabolism (sequential inhibition) leading to troubles in DNA synthesis.

59
Q

Sulfas/trimethoprim spectrum

A

Broad spectrum against many G+ and G-, also some parasites (i.e. Toxo) and Pneumocystis jiroveci

60
Q

Tetracyclines mechanism

A

Bind reversibly to 30S subunits, preventing attachment of aminoacyl-tRNA to ribosomal acceptribosomal or in RNA-ribosome complex usually bacterioSTATIC

61
Q

Name two drugs where both MIC and therapeutic drug monitoring are used…

A

Aminoglycosides Vancomycin - pay attention to MIC because there’s a range of effective doses and the higher required doses can cause toxicity problems

62
Q

Vancomycin mechanism

A

Vancomycin forms hydrogen bonds with D-Ala-D-Ala dipeptide, which inhibits transpeptidase and peptidoglycan crosslinks.

63
Q

Vancomycin spectrum

A

Gram positive ONLY. Cannot diffuse across LPS outer membrane of G-

64
Q

When reading a KB plate, what are conditions in which the inner “haze” is ignored and the ZOI is measured further out?

A
  1. Proteus will swarm in but it’s not actually growing
  2. Sulfonamides and trimethoprim disks may have an inner haze due to the organism population going through several doubling generations before inhibition.