Microbiology Exam Ii (Slides 16-17)

Front 1

Why is a high therapeutic ratio better than a low reading?

Back 1

A high therapeutic index is preferable to a low one: this corresponds to a situation in which one would have to take a much higher dose of a drug to reach the lethal threshold than the dose taken to elicit the therapeutic effect.

Front 2

What is Bacteriocidal and what is Bacteriostatic?

Back 2

Bacteriocidal kills the bacteria
Bacteriostatic stops bacteria growth

Front 3

Isoniazid is effective against what kind of bacteria?

Back 3

Mycobacteria

Front 4

What MBC: Minimum Bacteriocidal Concentration and Minimum Inhibition Concentration?

Back 4

MIC- The lowest concentration that inhibits visual growth in plates (colony/lawn formation) or liquid culture (turbidity or OD measurement)

MBC- The lowest concentration the kills 99.9% of bacteria in a given time

Front 5

What makes drug usually have a high therapeutic ratio?

Back 5

This is usually acquired because the targets mechanisms (enzymes/structures) that the host does not possess.

Front 6

What is the target of penicilin?

Back 6

Penicillin target transpeptidase enzymes which cross-link peptidoglycan. There are no human enzymes which are inhibited by penicillins. Penicillins are thus usually very well tolerated by humans in high amounts. Toxic effects may not be seen until the concentration is so high that it begins to precipitate.

Front 7

Describe how the Kirby-Bauer Assay helps to determine the MIC?

Back 7

Bacteria plated at high concentration so they will grow as a “lawn” on plate

Then place a antibiotic paper plate on the bacteria plate and see the variety in growth around that, zone of inhibition

Front 8

If you are using the bacteriostatic drugs, what are you relying on to kill the bacteria?

Back 8

The host but remember some sites do not have good immune clearence (endocardium, brain, spine) and will require bacteriocidal antibiotics

Front 9

What is an example of a site that is difficult for antibiotics to reach and a site that can concentrate antibiotics?

Back 9

Urinary tract-concentrate
Blood brain barrier-DIfficult

Front 10

What are the three main mechanisms to fight antibiotics?

Back 10

Permeability of antibiotic attacking the bacteria

Mutate the site the antibiotic attacks

Destroy the antibiotic (beta lactamase, CAT, AMEs)

Front 11

What is a mechanism that some bacteria use to keep antibiotics from entering the outer membrane, capsules or the peptidoglycan layer?

Back 11

Efflux pumps – transmembrane proteins that specifically remove antibiotics

Front 12

Concerning bacteria: natural selection + time + large population size =

Back 12

Resistance

Front 13

Peptidoglycan is a drug that similar to the structure of _ ____ and acts as a _______ _____ of enzyme(s) which cross link peptidoglycans (composed in part of D – alanine)
i.e. it binds the active site of transpeptidase

Back 13

D-Alanine
Competitive inhibitor

Front 14

How do beta lactamase attack beta lactams (penicillin) and where are they usually secreted?

Back 14

They will open the 4 membered ring in beta lactams and they are secreted into medium (gram pos) or stored in periplasmic space (gram neg)

Front 15

Name a beta lactam and a beta lactamase inhibitor?

Back 15

Amoxicillin (transpeptidase inhibitor) + clavulonate (lactamase inhibitor)

Front 16

What is a subclass of beta lactams that are among most widely used antibiotics?

Back 16

Cephalosporins

Front 17

Explain the importance of:
THF-Tetrahydrofolate

Back 17

Tetrahydrofolate is necessary for thymidine synthesis. The reaction dUMP → dTTP requires Tetrahydrofolate
Therefore, without THF, dTTP cannot be made, therefore DNA cannot be made.

Front 18

Why is sulfoamides effective?

Back 18

Sulfoamide inhibits the enzyme Dihydropteroate synthetase.

Dihydropteroate synthetase catalyzes the conversion of PABA to Dihydrofolate.

Dihydrofolate is a precursor of THF. With this gone dUMP → dTTP will not occur and DNA cannot be synthesized.

Front 19

Sulfonamides are structural analogs of ?

Back 19

PABA

Front 20

Bacteria cannot absorb folate they must make it. What do enzyme is responsible for this?

Back 20

Dihydrofolate synthetase

Front 21

Sulfa and Trimethoprim both interfer with folate production but what is the difference?

Back 21

Sulfa inhibits PABA to DHF
Trimethoprim inhibits DHF to THF

Front 22

The reaction of Dihydrofolate to Tetrahydrofolate is done by the enzyme?

Back 22

dihydrofolate reductase or DHFR

Front 23

What is usually the resistance against Trimethoprim ?

Back 23

Mutated or altered dihydrofolate reductase or DHFR.

Front 24

Penicillin + ________ are drugs used together because Drug A interferes with ability of bacteria to overcome effects of drug B.

Back 24

aminoglycosides

Front 25

Tetracyclines competes with ________ for binding to ____ ribosome

Back 25

tRNA
30S

For tetracyclines bacterial active transport system will increase cellular concentration

Front 26

How is resistance given for tetracyclines?

Back 26

Mutation of active transport system confers resistance

Front 27

How do the macrolides function?

Back 27

They bind 50S ribosomal subunit and sterically block progression of nascent peptide.

Front 28

How can bacteria become more resistant to macrolides (Erythromycin, Lincomycin)

Back 28

The bacteria ribosomes can become modified

Front 29

Describe how Rifamycin/Rifampin/Rifampicin functions?

Back 29

The Rifamycin/Rifampin/Rifampicin will bind to RNA polymerase and inhibit transcription. This is done by Rifamycin/Rifampin/Rifampicin displacing the Mg++ from the RNA polymerase.

Front 30

How can there be resistance from Rifamycin/Rifampin/Rifampicin?

Back 30

Modification of RNA polymerase

Front 31

What is Rifamycin/Rifampin/Rifampicin usually reserved for attacking?

Back 31

It is usually reserved for attacking TB in combination with isoniazid

Front 32

Rifamycin/Rifampin/Rifampicin is a fairly hydrophobic molecule, why is this a benefit to the human body?

Back 32

This is important because it allows the molecule to cross the blood brain barrier and Mycobacterial cell walls.

Front 33

Describe the function of Isoniazid

Back 33

Isoniazid inhibits a fatty acid synthase in Mycobacteria, meaning inhibits the production of mycolic acid. This antibiotic is bacteriocidal and will only effect mycobacteria (myco produce mycolic acid)

Front 34

What is the antibiotic will target fatty acid synthesis?

Back 34

Isoniazid

Front 35

What is the antibiotic will target cell wall synthesis?

Back 35

Penicillin and cephlaosporins

Front 36

What is the antibiotic will target RNA synthesis?

Back 36

Rifamycin, rifampicin

Front 37

What antibiotic targets Nucleic acid synthesis

Back 37

Trimethoprim
Sulfa

Front 38

What antibiotic targets DNA replication

Back 38

fluoroquinolones (DNA gyrase inhibitors)
AZT – chain terminator

Front 39

What antibiotic targets Protein synthesis

Back 39

macrolides - 50S subunit
Tetracycline – 30S codon:anticodon

Front 40

E.coli is ____trichous the spin of flagella determines the direction of movement.

Back 40

Multi

Front 41

If the flagella spins CCW the E.coli will go ______

Back 41

Forward

Front 42

If the flagella spins CCW the E. Coli will _______

Back 42

Tumble

Front 43

Describe the biased random walk

Back 43

This is the way in which the flagella will propel the E. Coli.

With an increase in attractants the frequency of run is increased and the frequency of tumbling is decreased.

With an increase in repellents the frequency of tumbles is increased and the frequency of runs is decreased

Front 44

What is the ratio of runs:tumbles in flagella?

Back 44

95:5

Front 45

What is the name for the following:
In a liquid medium, E. coli shows long straight “runs” followed by short tumbles, followed by another run in a different, random direction.

Back 45

Random walk

Front 46

Describe the structure of MCP's?
Methyl Accepting Chemotaxis Proteins

Back 46

MCPs are membrane spanning proteins with a binding domain on the periplasmic side and a cytoplasmic domain.
The cytoplasmic side will interact with CheW and CheA.

The periplasmic side will interact with attractors (amino acids and sugars).

Front 47

Describe how CheA starts the process of flagella start tumbling. Using CheB, CheY, CheZ.

Back 47

CheA has the chance of undergoing autophosphorylation
-ATP to ADP

Once phosphorylated it will then move the phosphate to CheB or CheY.

CheY phosphorylated will then diffuse away and cause the flagella motor to cause the tumbling to occur.

After a few seconds, cheZ removes the phosphate from cheY, and the flagella resumes CCW rotation (the cell swims straight again)

Front 48

What will attractants do to MCP's?

Back 48

This will inhibit the phosphorylation of CheA

Front 49

What will repellents do to MCP's?

Back 49

This will activate CheA

Front 50

What does the CheB function as in MCP'?

Back 50

CheB acts to adjust methylation levels on the MCP. This adjusts the sensitivity of the MCP to the current environment.

Front 51

Will repellents activate the demethylase activity of CheB?

Back 51

Yes

Front 52

If there is a high level of attractants, how will this affect the ratio of running:tumbling?

Back 52

This won't change the ratio 95:5