Bacterial resistance Flashcards

1
Q

How do bacteria inactive drugs?

A

They produce enzymes that destroy them

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2
Q

How are beta-lactam AB inactivated?

A

Cleavage of Beta-lactam ring

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3
Q

How are aminoglycoside AB inactivated?

A

Modified via acetylation, adenylation, or phosphorylation

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4
Q

How can bacteria decrease accumulation of AB?

A
  1. Mutate or lose porin channels which AB use to enter cells

2. Increase efflux of AB

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5
Q

What causes resistance to bind to fluoroquinolones?

  1. Mutations in DNA gyrase (A, B subunits
  2. Mutation in rpoB encoding beta subunit of RNA polymerase
  3. Resistance to beta-lactams
  4. Alterations in cross-linking of peptidoglycan
  5. Decreased access to ribosomes due to presence of ribosomal protective proteins (tet genes)
A
  1. Mutations in DNA gyrase (A, B subunits
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6
Q

What causes resistance to bind to Rifampin?

  1. Mutations in DNA gyrase (A, B subunits
  2. Mutation in rpoB encoding beta subunit of RNA polymerase
  3. Resistance to beta-lactams
  4. Alterations in cross-linking of peptidoglycan
  5. Decreased access to ribosomes due to presence of ribosomal protective proteins (tet genes)
A
  1. Mutation in rpoB encoding beta subunit of RNA polymerase
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7
Q

What causes resistance to bind to penicillin?

  1. Mutations in DNA gyrase (A, B subunits
  2. Mutation in rpoB encoding beta subunit of RNA polymerase
  3. Resistance to beta-lactams
  4. Alterations in cross-linking of peptidoglycan
  5. Decreased access to ribosomes due to presence of ribosomal protective proteins (tet genes)
A
  1. Resistance to beta-lactams
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8
Q

What causes resistance to bind to Vancomycin?

  1. Mutations in DNA gyrase (A, B subunits
  2. Mutation in rpoB encoding beta subunit of RNA polymerase
  3. Resistance to beta-lactams
  4. Alterations in cross-linking of peptidoglycan
  5. Decreased access to ribosomes due to presence of ribosomal protective proteins (tet genes)
A
  1. Alterations in cross-linking of peptidoglycan
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9
Q

What causes resistance to bind to Tetracycline?

  1. Mutations in DNA gyrase (A, B subunits
  2. Mutation in rpoB encoding beta subunit of RNA polymerase
  3. Resistance to beta-lactams
  4. Alterations in cross-linking of peptidoglycan
  5. Decreased access to ribosomes due to presence of ribosomal protective proteins (tet genes)
A
  1. Decreased access to ribosomes due to presence of ribosomal protective proteins (tet genes)
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10
Q

How could you treat resistant infections due to inactivation of drug?

A

Incorporate Beta-lactamase inhibitors w/ Beta-lactams

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11
Q

How does incorporating Beta-lactamase inhibitors w/ Beta-lactams help treat resistant infections due to inactivation help?

A

Prevents hydrolysis of antibiotic

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12
Q

Clavulanic MOA?

A

Irreversible binding of Beta-lactamse enzyme (Suicide inhibitor)

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13
Q

How do you treat resistant infections due to modification of drug?

A

Novel chemical synthesis of aminoglycoside to prevent modifications by bacterial enzymes

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14
Q

What is an analog to semisynthetic tetracycline derivative minocycline that is not affected by ribosomal protective + tetracycline-specific efflux?

A

Tigecycline

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15
Q

How would you get around efflux mechanisms?

A
  1. Use Tigecycline

2. Use efflux inhibitors (especially useful w/ fluorquinolones)

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16
Q

What is an alternate if porin mutations exist?

A

Use siderophore uptake systems (iron uptake system)

17
Q

How do you get around a drug not being able to bind to target/reduced affinity to binding spot on bacteria?

A

Alter AB structure to bind or restore affinity to target while retaining antimicrobial activity