Antimicrobial Agents & Resistance - Richardson Flashcards

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1
Q

What is MIC?

A

Minimum Inhibitory Concentration - Lowest concentration at which bacteria cannot grow

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2
Q

What is MBC?

A

Minimum Bactericidal Concentration - Lowest concentration which causes 1000-fold reduction in bacteria.

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3
Q

What is the difference between bacteriostatic and bactericidal antibiotics?

A

Static = Inhibits growth allowing immune response to clear the infection.

Cidal = Kills bacteria

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4
Q

Do antibiotics kill bacteria by generating ROS?

A

NO.

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5
Q

What are the 3 ways bacteria evolve resistance to drugs?

A
  1. Inactivate the drug
  2. Alter the drug’s target
  3. Alter exposure to the drug
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6
Q

Why are gram negative bacteria better at clearing cell-wall antibiotics?

A

They have a cell membrane and a cell wall allowing them to better efflux. They also can change porins allowing them to not uptake drug. More ways to alter exposure.

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7
Q

Why can’t gram positive bacteria alter their exposure to cell-wall antibiotics?

A

They don’t have an outer membrane protecting their cell wall so they can’t efflux antibiotics or alter uptake via porins. They can only alter target or secrete inactivating enzymes.

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8
Q

What is the target of beta-lactam antibiotics?

A

Trans-peptidases in the bacterial cell wall. This disrupts cell-wall integrity.

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9
Q

What links sugars together in bacterial cell walls?

A

Transglycosylases

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10
Q

What are penicillin binding proteins?

A

Proteins that polymerize and stabilize peptidoglycan of bacterial cell-walls.

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11
Q

What is the mechanism of beta-lactams?

A

B-lactams mimic D-ala-D-ala in peptidoglycans preventing penicillin binding protein from cross-linking peptidoglycan

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12
Q

How do beta-lactamases degrade beta-lactams?

A

Beta-lactamases hydrolyze the same bonds as PBPs allowing bacteria to form peptidoglycan cross-links regardless of drugs.

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13
Q

What is alternative way that bacteria can evade B-lactam drugs?

A

They have PBPs that don’t bind B-lactams but still have transpeptidase activity such as MRSA and N. gonorrhea

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14
Q

What did N. gonorrhea evolve to become resistant to penicillin?

A
  1. Mutated porins decreases drug uptake
  2. Constitutively expressed efflux pumps
  3. Altered PBPs
  4. B-lactamases
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15
Q

What are the targets of glycopeptide antibiotics?

A

They cap D-ala-D-ala so that it cannot interact with transpeptidases. Ex. Vancomycin

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16
Q

Mechanisms for resistance of glycopeptides such as vancomycin:

A

Some bacteria can compose their cell walls of D-ala-D-lac cross-links which vancomycin cannot recognize.

17
Q

Which gene encodes resistance to methicillin?

A

mecA

18
Q

How do bacteria evolve drug resistance before drugs were even invented? Then how is it selected for?

A

We utilize antibiotics derived from soil bacteria. Pathogenic bacteria can pick up genes via plasmid or phage from other antibiotic-producing soil bacteria and confer resistance. Clinical use of antibiotics has redistributed antibiotic resistance from their natural origin to human pathogens.

19
Q

Three ways bacteria pick up genes?

A
  1. Transformation - Raw DNA (plasmids).
  2. Transduction - Infection by phage
  3. Conjugation - Pili