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Clinical Micro > Antibiotic Classes and Resistance > Flashcards

Antibiotic Classes and Resistance Flashcards

1
Q

What are the 3 types/names of cell wall synthesis inhibitors?

A
  1. ß-lactams
  2. Glycopeptides
  3. Fosfomycin
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2
Q

What are the 3 Classes of ß-lactams?

A
  1. Penicillins
  2. Cephalosporins
  3. Carbapenems
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3
Q

What is the mode of action of ß-lactams? What stuctural feature do they all share? What are the analogous to?

A

competitive inhibition
All have a ß-lactam ring
Are analogous to D-ala-D-ala

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4
Q

What is the target of ß-lactams? How do they target them?

A

Penicillin binding proteins (PBPs)

  • acts as D-ala-D-ala analogues and bind to the PBP
  • the PBPs are now occupied and transpeptidation is inhibited
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5
Q

What are 4 methods of ß-lactam resistance? Which is the most common?

A
  1. Production of ß-lactamase (most common)
  2. Altered PBPs
  3. Novel PBP
  4. Altered permeability (mainly gram negatives)
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6
Q

How does ß-lactamase work?

A

Cleaves the ß-lactam ring which inactivates the drug

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7
Q

What are two important ß-lactamase inhibitors?

A

Clavulanic acid and Tazobactam

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8
Q

Which drug that we discussed is part of the Glycopeptides?

A

Vancomycin

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9
Q

What types of bacteria are susceptible to Vancomycin

A

Gram positives only

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10
Q

What is the mode of action for glycopeptides?

A

bind to the terminal D-ala of nascent cell wall peptides and prevents cross-linking of these peptide to form mature peptidoglycan

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11
Q

How have bacteria developed Vancomycin resistance?

A
  • D-ala-D-ala target is altered - bacteria substitutes D-lac for D-ala- vancomycin CANNOT bind
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12
Q

What two bacteria are the primary concern for Vancomycin resistance?

A
  1. Staphylococcus aureus

2. Enterococcus

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13
Q

How does fosfomycin work?

A

Blocks the enzyme enol-pyruvyl transferase. Blocks condensation of UDP-N-acetylglucosamine with p-enolpyruvate

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14
Q

What is the spectrum of activity for fosfomycin?

A

Broad spectrum : both gram positives and negatives

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15
Q

What is fosfomycin used to treat primarily ? Caused by what organisms?

A

Uncomplicated cystitis in women

- caused by E.coli / E.faecalis

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16
Q

What does fosfomycin often retain activity against?

A

Bacteria that produce extended spectrum ß-lactamases (ESBLs)

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17
Q

What do the fluoroquinolones inhibit?

A

DNA synthesis

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18
Q

What is the difference between the classes of Cephalosporins? How do they differ in activity?

A

1st gen are very good against gram positive bacteria

As you increase generations you tend to lose gram positive activity and gain gram negative activity

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19
Q

Are fluoroquinolones time or concentration dependent? Bacteriocidal or bacteriostatic?

A

Concentration dependent and bactericidal

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20
Q

What is an example of a 2nd generation fluoroquinolone? what is it good against? what made it different from the 1st generation?

A

Addition of fluorine was a big change from the 1st generation

Ciprofloxacin is a good example

Broader spectrum and a very good anti-pseudomonal

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21
Q

What is an example of a 3rd generation fluoroquinolone? What is different between the 2nd generation and the 3rd?

A

The 3rd have better gram positive activity
- also have anaerobic activity (?)

Moxifloxacin is a good example

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22
Q

What are fluoroquinoles good acting against on the whole?

A

Atypical bacteria like mycoplasma (Chlamydia?)

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23
Q

What are the two specific targets of the fluoroquinolones?

A
  1. DNA gyrase

2. Topoisomerase IV

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24
Q

What do the fluoroquinolones do when they act on DNA gyrase?

A

prevent the DNA from reannealing

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25
Q

Both DNA gyrase and Topo IV are ___ enzymes

A

tetrameric

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26
Q

What causes “de novo” resistance to the fluoroquinolones ? (4 things)

A
  1. Spontaneous mutations in parC and gyrA - results in AA substitution = reduced affinity
  2. Over expression/up regulation of intrinsic efflux pumps
  3. Down regulation of porin channels in gram negatives
  4. Qnr production
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27
Q

What is Qnr?

A

protein that binds to and protects topoisomerase

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28
Q

How can bacteria acquire resistance to fluoroquinolones?

A

acquisition of resistance determinants from viridans streptococci

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29
Q

Fluoroquinolones have very good ___ bioavailability

A

oral

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30
Q

Where do the fluoroquinolones typically concentrate?

A

urine, kidney, prostrate, bile, lung, and macrophages

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31
Q

Which fluoroquinolone does not concentrate in the urine?

A

Moxifloxacin

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32
Q

What are two adverse effects of the fluoroquinolones? Who are they not used to treat?

A
  1. hyper/hypoglycemia
  2. cartilage toxicity and tendon rupture

Don’t use for children

33
Q

What are two important situations to use fluoroquinolones?

A
  1. Atypical or gram negative infections like pseudomonas

2. Complicated UTIs

34
Q

What are 4 other situations you would want to use fluoroquinolones?

A
  1. Intra-abdominal infections (rarely1st line) - combine with metronidazole
  2. Gastro-intestinal infections
  3. Hospital acquired Respiratory tract infections
  4. Community acquired (complicated) Respiratory tract infections
35
Q

What is metronidazole the go to drug for? give some examples

A

Anaerobic or parasitic infections

C. difficile colitis
Trichmonas vaginitis and BV
H. pylori (in combination)

36
Q

What is the mechanism of action of metronidazole?

A

Inhibits nucleic acid synthesis by disrupting /damaging DNA through the production of short lived toxic intermediates or free radicals under anaerobic (reducing) conditions

37
Q

What are some side effects of Metronidazole use?

A 
GI intolerance
Antabuse effect
Peripheral neuropathy
Metallic taste 
Black/brown discoloration of urine
38
Q

What are the 3 Macrolides we talked about?

A

Erythromycin, Clarithromycin, Azithromycin

39
Q

What is the specific target of the macrolides?

A

Binds to the 50S subunit of the bacterial ribosome

40
Q

What is the mechanism of action of the Macrolides

A
  1. blocks growth of nascent peptide chain by stimulating dissociation of the peptidyl-tRNA from the ribosome
  2. Also inhibits assembly of new ribosomes
41
Q

What does MLS stand for?

A

Macrolide, Lincosamide, Streptogramin

42
Q

What is the M phenotype?

A

presence of efflux pump, means that the bacteria are only resistant to macrolides

43
Q

What is the MLS phenotype?

A

resistant to Macrolides, Lincosamides, Streptogramins due to activation of the erm gene which leads to AA substitutions/alterations in the 50S target site

44
Q

What 3 first line uses for Macrolides?

A
  1. Mild-moderate community acquired pneumonia
  2. Pertussis
  3. Atypical pathogens like mycoplasma and chlamydia
45
Q

What are 3 second line uses for Macrolides?

A
  1. Penicillin allergic patients
  2. URTIs
  3. C. jejuni gastroenteritis
46
Q

What antibiotic is most often associated with C. difficile colitis

A

Clindamycin

47
Q

What are 3 clinical uses of Clindamycin

A
  1. Anaerobic infections (typically gram neg)
  2. Gram positive infections (like staph)
  3. C. perfringens in penicillin allergic patient
48
Q

What 5 drugs/group of drugs inhibit protein synthesis by binding to the 50S subunit?

A
  1. Macrolides
  2. Clindamycin
  3. Linezolid
  4. Chloramphenicol
  5. Streptogramins
49
Q

What are the 3 Tetracyclines that we discussed?

A

Tetracycline, Doxycycline, Minocycline

50
Q

Where do tetracyclines target? How do they bind?

A

Bind reversibly to the 30S subunit

51
Q

What are 3 basic mechanisms of resistance that bacteria use against the tetracyclines?

A
  1. Energy dependent efflux
  2. Enzymatic inactivation
  3. Ribosomal protection
52
Q

What are two types of infections that tetracyclines are excellent against?

A
  1. Atypical infections

2. Animal borne

53
Q

What kind of infections are tetracyclines ok at combatting? What is an example?

A

most gram positives

ex: CA-MRSA

54
Q

What are some adverse effects of tetracyclines?

A

discoloration of teeth
photosensitivity
depression of skeletal growth
esophageal ulceration

55
Q

Who can’t be treated with tetracyclines? why?

A

Children under 12 or their teeth will be discoloured for life

56
Q

What kind of antibiotics are the aminoglycosides?

A

Natural and semi synthetic

57
Q

What are 4 examples of aminoglycosides?

A

Streptomycin, Gentamicin, Tobramicin, Amikacin

58
Q

What are the spectra of activity for aminoglycosides?

A

excellent: gram negatives including pseudomonas
good: gram positives

59
Q

What kind of killing do the aminoglycosides use?

A

Concentration dependent and bactericidal

60
Q

What kinds of infections cannot be treated with aminoglycosides and why?

A

cannot be used for anaerobic infections or abscesses. Need to be actively transported into the cell in a process that required oxygen

61
Q

What is the target of aminoglycosides? How do they bind?

A

Bind irreversibly to the 30S subunit

62
Q

What is the mechanism of entry into the cell for the aminoglycosides? What is the rate limiting step? What blocks it?

A

Entry through inner membrane via an energy dependent transport system (electron transport)
This step is rate limiting and blocked by divalent cations and anaerobiosis

63
Q

What is the most common form of resistance to the aminoglycosides?

A

Enzymatic modification

64
Q

What are 2 other ways that bacteria have developed resistance to aminoglycosides?

A
  1. Altered ribosome binding sites

2. reduced uptake or decreased cell permeability

65
Q

What are the two main adverse side effects of aminoglycoside use (hint: what are they toxic to?) What causes these side effects?

A

Can interfere with mammalian protein synthesis at high concentrations

  1. ototoxic: both cochlear and vestibular
  2. nephrotoxic: proximal tubule damage
66
Q

What 5 situations would you want to treat with aminoglycosides?

A
  1. Complicated UTIs (Pyelonephritis)
  2. Mixed infections without abscess formation
  3. Endocarditis treatment (synergy Enterococcus)
  4. Pseudomonas infections
  5. For resistant Gram negative bacilli
67
Q

What drug blocks folic acid synthesis?

A

Trimethoprim/sulfamethoxazole (Septra, TMP/SMX)

68
Q

What bacteria are TMP/SMX effective against?

A

good gram negative, some gram positive

69
Q

How does TMP/SMX work?

A

Blocks folic acid synthesis at two different steps

- not synergistic

70
Q

What is the pathway to folic acid synthesis and which of TMP/SMX acts on each stage?

A
  1. PABA —-> dihydrofolic acid
    - this step blocked by Sulfonamides (SMX)
  2. Dihydrofolic acid —> tetrahydrofolic acid
    - this step blocked by Trimethoprim (TMP)
71
Q

What are the 2 mechanisms of resistance to TMP/SMX? Which is more common?

A
  1. Chromosomal:
    - metabolic bypass
    - over expression of dihydrofolate reductase
  2. Plasmid (most common)
    - drug resistant variants of DHFR / DHPS
72
Q

What was TMP/SMX commonly used for but not has high rates of resistance?

A

uncomplicated UTIs

73
Q

What is TMP/SMX a very active agent against?

A

anti-Staphylococcal agent (CA-MRSA)

74
Q

What are two antibiotics that we discussed with activity against the bacterial cell membrane? What class of bacteria do they each act on?

A
  1. Colistin (gram negatives, some gram positive activity )

2. Daptomycin (gram positive agent)

75
Q

How does Colistin work ? what is it best used to treat?

A

Displaces divalent cations from phosphate groups of membrane lipids
Disrupts outer membrane
Useful in treating MDR gram negative infections

76
Q

What is Colistin toxic against?

A

Renally and neurologically toxic

77
Q

What is the one kind of infection that only Colistin can be used to treat?

A

CRE infections

78
Q

How does Daptomycin work? What is it useful in treating?

A

Insertion into bacterial cell membrane
Rapid membrane depolarization and K+ ion flux
Bactericidal concentration-dependent killing
useful against MRSA

79
Q

What can Daptomycin not be used to treat? Why?

A

Cannot be used for RTIs because lung surfactin will inactivate the drug

Clinical Micro (28 decks)

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