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MICRO 121 > Lecture 6: Antimicrobial Compounds and Resistance Mechanisms > Flashcards

Lecture 6: Antimicrobial Compounds and Resistance Mechanisms Flashcards

1
Q

Bactericidal

A

“cidal” - kills susceptible bacteria - host responses not needed

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2
Q

Bacteriostatic

A

“static” inhibits bacterial growth and relies on host defences to clear the bacteria

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3
Q

Narrow spectrum antibiotics

A

active against a small group of bacteria (good)

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4
Q

Broad spectrum antibiotics

A

Active against a much wider variety of bacteria (bad)

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5
Q

Resistance

A

When an organism no longer responds to a therapy OR is associated with failure in vivo

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6
Q

Sensitive

A

When an organism responds to an antimicrobial and has activity in vivo

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7
Q

Antimicrobial Targets

A

Cell Wall Synthesis
- Beta Lactams: Penicillins, cephalosporins, carbapenems, monobactams
- Vancomycin Bacitracin
- Cell Membrane: Polymyxins

Nucleic Acid Synthesis
- Folate synthesis: Sulfonamides; Trimethoprim
- DNA Gyrase: Quinolones
- RNA Polymerase: Rifampin

Protein Synthesis
- 50S subunit: macrolides, clindamycin, linezolid, chloramphenicol, streptogramins
- 30S subunit: Tetracyclines, Aminoglycosides

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8
Q

Cell Wall Synthesis Inhibitors Beta-Lactam antibiotics

A
  • The beta-lactam ring is the central component of all beta-lactam antibiotics
    Antibiotic in this class include: Penicillins, Amoxicillin, Cephalosporins, Minocyclines, and Carbapenems
  • They work by inhibiting cell wall synthesis
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9
Q

Cell wall components and Beta-lactam antibiotics

A
  • The transpeptidase enzyme crosslinks the peptidoglycan
  • Beta lactams interfere with binding
  • Cell wall stays permeable, then bacteria dies
  • Beta-lactam antibiotics bind to transpeptidase enzymee complex and blocks this reaction
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10
Q

Most common Penicillins

A
  • PenicillinG
  • PenicillinV
  • Cloxaclillin
  • Amoxicillin
  • Piperacillin
  • Most specific, focus on certain parts
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11
Q

Common Cephalosporins
1. 1st Gen
2. 2nd Gen
3. 3rd Gen

A
  1. Ampicillin
  2. Cefazolin
  3. Ceftazidime, Ceftriaxone, Cefixime
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12
Q

Common Carbapenems

A
  • Ertapenem
  • Meropenem
    *Best and most broad, most activity, last line of drugs
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13
Q

Beta-lactam Antibiotics

A
  • Active in both gram positive and gram negatives
  • Penicillin and ampicillin are narrow spectrum
  • 1st gen cephalosporins are narrow spectrum. 3rd and 4th generation of cephalosporins have broader coverage and usually used for more resistant organisms
  • Carbapenems are very broad spectrum antibiotics and used as antibiotics of last resort (BROADEST)
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14
Q

Glycopeptides: Non Beta-Lactam Cell wall active agents

A
  • Glycopeptides act on the cell wall of GRAM POSITIVE organisms
  • Stops the extension of the peptidoglycan unit of the bacterial cell wall
  • Drugs in this class include: Vancomycin and Teicoplanin
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15
Q

Protein Synthesis Inhibitors

A
  • Binds parts of the ribosomes
  • Ribosomes in bacteria are structures that make proteins from nucleic acids
  • Ribosomes have subunits called 30S and 50S (70S ribosome in prokaryotic cells)
  • Antibiotics bind the 30S and 50S subunit of ribosomes and stop protein synthesis in bacteria
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16
Q

Protein Synthesis Inhibitor Famalies

A
  1. Tetracyclines (block the attachment of tRNA to the ribosome - important)
    Ex: Demeclocycline
  2. Macrolides (prevent the continuation of protein synthesis - important)
    Ex: Azithromycin - good for pneumonia
  3. Chloramphenicol (prevents peptide bonds from being formed - less important than the other two)
17
Q

Nucleic Acid Inhibitors: Fluoroquinolones

A
  • Stop protein synthesis by messing with nucleic acid
  • Prevents DNA RNA replication by targeting
    Prevents DNA gyrase or RNA topoisomerase
18
Q

Fluoroquinolones

A
  • Excellent drugs with a broad spectrum of activity
  • Good tissue penetration
    Example: Moxifloxacin
19
Q

Metabolic Inhibitors

A
  • Trimethoprim/Sulfamethoxazole (Septra, Bactrim)
  • Inhibitors of the active form of folic acid (tetrahydrofolic acid)
  • Trimethoprim - structural analogue of DHF (Dihydrofolic acid) and competitive inhibitor of dihydrofolate reductase
  • Sulfamethoxazole - structural analogue of PABA and competitively inhibits synthesis of DHF
20
Q

Intrinsic Resistance

A

You don’t have to do anything for it (Like how your skin is waterproof)

21
Q

Acquired Resistance

A
  • Developed and got from other things (“Like a jacket” to keep you warm, can be shared, but have to go get it)
22
Q

Testing for resistance

A

We won’t test, we’ll analyze results
We care about you acquired because you want to control the spread
- Antibiotic testing is done in vitro (in glass)
- Data will show what will be effective or ineffective
- The interpretations of the testing are reported as either Sensitive (S): patient will get better, Intermediate (I): up the antibiotic dose, or Resistant (R): patient will not get better
- If organism grows in presence of antibiotics - then R, if organism doesn’t grow then S

23
Q

Microbroth Dilution

A
  • The last well before growth is seen is the Minimum Inhibitory Concentration (MIC)
  • Take concentration of bug and drug, where the lack of growth is the concentration that is MIC
  • Different concentrations of antibiotics from L of the plate to the R
  • Suspension of bacteria added to the plate and incubated
24
Q

Bacterial Resistance Characteristics

A
  • Inherited or acquired
  • The generation of mutation(s) is partly because of the short replication times - some bacterial generations are as short as 20 min
  • Frequency of mutations is about 1 in 10 million cells
  • A colony of bacteria has 100 million cells - potential for up to 10 mutation events in one colony
25
Q

4 Resistance Mechanisms + what is a resistance mechanism

A
  • Resistance genes can be on the bacterial chromosome (intrinsic) or on a motile gene element called a plasmid (circular strand of DNA)
    1. Efflux pump - bug pumps out antibiotics, reduced permeability, changes thickness and size
    2. Reduced permeability
    3. Enzymatic inactivation - bacteria makes enzyme that breaks down
    4. Altered binding site - antibiotic binds to site, if site is altered it will not bind
    (1 and 2 resistance mechanism can’t be passed on, 3 and 4 is the one to be nervous about because it means limiting options for patient
26
Q

Bacterial Resistance

A
  • Resistant mechanisms often have a resistance mechanism often have a costs associated to them (Fitness or metabolic)
  • 2 types of resistant mechanisms - either “always on” (usually acquired) or “inducible” (intrinsic - following antibiotic exposure)
  • Lack of selective pressure will result in the loss of a particular resistance mechanism (particularly the acquired resistance phenotype)
  • There are several ways that resistance mechanisms may be shared in inter or intra species (FINISHED AT SLIDE 23)

MICRO 121 (19 decks)

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