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Disease & Defense > LEC 35 Antimicrobials III > Flashcards

LEC 35 Antimicrobials III Flashcards

1
Q

What are the 3 antibiotic targets inside the cell?

generally speaking

A
  1. Ribosome
  2. Metabolic Enzymes
  3. DNA
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2
Q

What are the two subunits of the prokaryotic ribosome?

A
  • 30S
  • 50S

Together they form a 70S Ribosome

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3
Q

What are the subunits of the eukaryotic ribosome?

A
  • 60S
  • 40S

Together, they make an 80S ribosome

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4
Q

How do tetracyclines work?

A
  • Reversibly bind 30S subunit preventing formation of the initiation complex
  • Bacteriostatic
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5
Q

What are some examples of tetracyclines?

A
  • Tetracycline
  • Minocycline
  • Doxycycline
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6
Q

What is the spectrum of tetracyclines?

A

Broad-spectrum including
* Mycoplasma pneumoniae (no cell wall)
* Rickettsia, Chlamydia (intracellular pathogens)
* Borrelia (Lyme disease)

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7
Q

What is the number one reason for tetracycline resistance?

A
  • Acquisition of tet transport genes which allow the bacteria to form the drug efflux pump
  • Doesn’t matter if the drug gets in the cell, bc it is pumped right back out
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8
Q

Which tetracycline is less subject to export by the drug efflux pump?

A

Minocycline

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9
Q

What is the new semisynthetic glycylcycline and why was it developed?

What’s its MOA?

A
  • Tigecycline (Tygacil)
  • Developed to overcome efflux pumps
  • Blocks tRNA binding necessary for protein synthesis
  • Also Broad Spectrum like other tetracyclines

Binds 30S subunit more efficiently than other tetracyclines

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10
Q

How do aminoglycosides work?

A
  • Bind the 30S subunit
  • Some are bactericidal and some are bacteriostatic
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11
Q

What are some of the bactericidal aminoglycosides?

A
  • Streptomycin
  • Kanamycin
  • Neomycin
  • Amikacin
  • Gentamicin
  • Tobramycin

Notice the -mycin/micin endings

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12
Q

Which two antibiotics end in -mycin but are NOT aminoglycosides?

A
  • Erythromycin
  • Vancomycin
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13
Q

Which aminoglycoside is bacteriostatic?

A

Spectinomycin

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14
Q

What is the main way that resistance to aminoglycosides happens?

A
  • Acquired resistance: modification of the abx
  • Transferases (acetyl, adenyl, phospho)
  • Effect is abx dependent (a modification that inactivates one aminoglycoside may have no effect on another aminoglycoside)
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15
Q

How does chloramphenicol work?

A
  • Binds 50S subunit and prevents elongation of the peptide chain

Mostly topical use d/t toxicity (eye drops)

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16
Q

How does resistance to chloramphenicol occur?

A
  • Modification of antibiotic
  • contains a gene (CAT) for chloramphenicol acetyltransferase
  • acetylates abx preventing it from binding the subunit
17
Q

What 3 groups are included in MLS Abx?

A
  • Macrolides
  • Lincosamides
  • Streptogramin
18
Q

How do the MLS abx work?

A

Bind the 50S subunit of the intact ribosome and inhibit translocation of the ribosome along the RNA

19
Q

What are some examples of macrolides?

A
  • Erythromycin
  • Azithromycin (z-pack)
  • Clarithromycin
20
Q

What is an example of a lincosamide?

A

Clindamycin

21
Q

What is are some examples of streptogramins?

A

Quinupristin + Dalfopristin = streptogramin A & B = Synercid

All same drugs, just different names and a combo drug

22
Q

How does resistance to MLS abx occur?

A
  • Modification of 50S subunit target NOT the abx - methylation of 23S rRNA
  • acquisition of gene, erm. (erythromycin resistance methylase)
  • causes reduced affinity for the abx
23
Q

How do oxazolidinones (Zyvox/linezolid) work?

A
  • Binds 50S subunit and inhibits formation of 70S initiation complex
  • Inhibits formation of 1st peptide bond
  • Bacteriostatic

Resistance: modification of 23S rRNA

24
Q

Why is tedizolid better than linezolid?

A
  • 4-6 times more potent against staphylococci and enterococci
  • active against linezolid resistant staphylococci
25
Q

Why are the oxazolidinones important?

A

Both linezolid and tedizolid have at least some activity against VISA and VRSA

26
Q

What enzyme controls DNA supercoiling?

A

DNA gyrase

along with other topoisomerases

27
Q

Why is DNA gyrase an effective drug target?

A
  • All cells have DNA gyrase, but bacterial DNA gyrase is more sensitive
  • Abx bind at concentrations lower than that required to damage mammalian topoisomerases
28
Q

What are some examples of fluorquinolones?

A
  • norfloxacin
  • ciprofloxacin
  • levofloxacin
  • gatifloxacin
29
Q

Why are quinolones (nalidixic acid) not used anymore?

A

widespread resistance

30
Q

How do fluoroquinolones work?

A

DNA gyrases inhibitors

31
Q

What is the spectrum of fluoroquinolones?

A
  • Broad-spectrum including mycobacterium
  • Effective against intracellular pathogens (concentrated inside phagocytic cells)
  • Norfloxacin is concentrated in urine making it good for UTIs
32
Q

How does Rifampin work?

A
  • binds beta subunit of DNA-dependent RNA polymerase and prevents binding to the promoter
  • Does NOT impair mammalian RNA polymerase
33
Q

What’s the spectrum of Rifampin?

A
  • Gram-positive and Mycobacterium
  • Cornerstone drug for TB
34
Q

Why are gram-negatives intrinsically resistant to Rifampin?

A

hydrophobic drug cannot cross outer membrane

35
Q

How does acquired resistance to Rifampin occur?

A
  • a single step mutation in the gene encoding the beta subunit of RNA polymerase
  • Rifampin RARELY USED ALONE (if ever)
36
Q

Why is tetrahydrofolate production a good drug target?

A
  • Mammalian cells get THF from the diet but bacteria have to make it
  • Required for biosynthesis of amino acids and nucleic acids
37
Q

How do sulfonamides work?

A
  • competitive inhibition of dihydropteroate (DHPS)
  • partial shutdown of THF synthesis (bacteriostatic)
38
Q

How does Trimethoprim work?

A
  • competitive inhibition of dihydrofolate reductase (DHFR)
  • partial shutdown of THF synthesis
39
Q

Why are sulfonamides and trimethoprim always used together?

A

They effectively shut down THF synthesis making them bactericidal when used together

Disease & Defense (37 decks)

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