Microbiology Ch 5 Biological Basis For Antibacterial Action

Front 1

MOA of sulfonamide

Back 1

Addition rxn to PABA inhibits synthesis of Dihydropteroic acid to folic acid

Front 2

Type of inhibition of sulfonamide on PABA

Back 2

Competitive

Front 3

Folic Acid's effect on sulfa drugs

Back 3

Non-Competitive inhibitor:
This is because as long as the bacterium has enough folate to satisfy growth requirements, no amount of sulfa could inhibit its growth. This is because Sulfa's MOA stops the synthesis of folate and by supplying exogenous folate, you can overcome this.

Front 4

Sulfa drugs inhibit the production of what vitamin? How?

Back 4

Folic acid:
Inhibition of PABA's addition rxn to DHPA stops folate synthesis and thus the coenzymes that contain it.

Front 5

Why do sulfonamides not affect the human body cell production of folic acid

Back 5

The human body requires preformed folic acid and thus does not synthesize folic acid.

Front 6

Does taking a folic acid supplement affect the efficacy of sulfa drugs?

Back 6

No
Bacteria can synthesize folic acid, however, they lack a system to uptake preformed folic acid and cannot benefit from its presence in the environment.

Front 7

Due to their cost, wide spectrum antibiotics should be considered only when

Back 7

When the etiological agent cannot be determined before therapy begins or for immunocompromised pts.

Front 8

Drug of choice for uncomplicated UTI

Back 8

Nitrofurantoin:
Concentrated in the urine. However, not effective for infections of blood or tissue

Front 9

Drug whose action may harm host cell membranes but is approved for topical infections

Back 9

Polymyxin and nystatin

Front 10

Drug whose MOA is inhibition of the enzyme DHFR (dihydrofolate reductase). Why is this drug not toxic to humans

Back 10

Trimethoprim: It is bactericidal in very small amounts that do not affect humans

Front 11

Difference in the MOA of sulfa and trimethoprim

Back 11

Sulfa blocks the synthesis of folic acid, whereas trimethoprim blocks the function of folic acid.

Front 12

β-Lactams are extremely selective because? Side effect?

Back 12

They affect the synthesis of murein, which is not present in humans
Destroy the normal colonic flora which may lead to colitis

Front 13

How are β-Lactam antibiotics modified to become “broad spectrum”? What bacteria is this targeted against?

Back 13

Modification of the β-Lactam rings and their side chains
Is able to also target Gram negative bacteria

Front 14

3rd generation cephalosporins are particularly useful in treatment of what organism? Why?

Back 14

Gram negative meningitis
Penetrate into the CNS

Front 15

Bactericidal action of β-lactams requires what steps?

Back 15

1. Association with the bacteria
2. Penetration through the outer membrane and the periplasmic space (Gram-)
3. Interaction with penicillin binding proteins on the cytoplasmic membrane
4. Activation of an autolysin that degrades the cell wall murein

Front 16

Principal mechanism to resistance of Penicillin and cephalosporins

Back 16

Elaboration of B-lactamases that cause hydrolysis of B-lactam ring

Front 17

Produce extracellular B-Lactamases. Can their resistance be overcome with increasing the dose of antibiotics?

Back 17

Gram+
B-Lactamases are made upon induction of antibiotics. These enzymes increase as the amount of antibiotics increases. As a result, resistance is usually not overcome.

Front 18

Contain B-Lactamases that are found in the periplasm or bound to the inner membrane. Can the resistance be overcome?

Back 18

Gram-
These enzymes are produced constitutively and may be overcome by large doses of antibiotics

Front 19

Inhibits peptidoglyan chain elongation by binding to D-ala-D-ala terminal peptides. Resistance?

Back 19

Vancomycin
Change in binding site in the peptidoglycan target due to acquisition of plasmid borne genes. Most often from Enterococcus organism. The terminal peptidoglycan percursor is changed to D-ala-D-lac.

Front 20

Carries the gene coding for B-lactamase, which hops to other strains of gonococci and to other aerobic gram- bacteria

Back 20

transposon

Front 21

MRSA achieves resistance via

Back 21

Altered penicillin-binding-proteins fail to bind to B-lactams. Occurs in Gram+.

Front 22

Drug that was specifically designed to resist staphylococcal B-lactamase

Back 22

Methicillin
Has now been affected by altered PBP's and has reduced efficacy

Front 23

Bacterial tolerance causing relapse of bacterial infections

Back 23

Partial resistance called tolerance that leads to bacteriostatic effects due to a lack of suicidal autolysin in these strain

Front 24

Mechanism of resistance to Flouroquinolones

Back 24

Mutations in genes encoding DNA gyrase and topoisomerase IV, which decreases binding.

Front 25

Quinolones inhibit what enzyme in Gram+ bacteria? Gram-?

Back 25

DNA Gyrase
Topoimerase IV

Front 26

MOA of linezolid

Back 26

Bind to the 50s subunit of ribosomes to prevent translation and initiation of protein synthesis

Front 27

MOA of antiribosomal antibiotics

Back 27

1. Penetration of outer membrane of Gram-
2. Association with a two-stage active transport system in the cell membrane
3. Binding to the 30s ribosome subunit to inhibit protein synthesis, at the initiation step, to promote miscoding by the ribosomes and the production of nonsense proteins.

Front 28

Mechanism of resistance to Aminoglycosides

Back 28

Modification enzymes by the addition of acetyl, adenyl, or phosphoryl groups. These enzymes are encoded by genes carried on plasmids

Front 29

MO resistance to tetracycline

Back 29

Efflux pump pushes drug out of cell

Front 30

MO resistance to macrolides

Back 30

Methylation of the 23S ribosomal RNA by a methylase (from a plasmid gene, induced by the presence of a macrolide), which renders the 50S subunit resistant