How does size make Gentamicin an effective antibiotic?
It cannot enter the eukaryotic membrane and thus only acts on extracellular microbes.
Why do you see a sudden drop in turbidity when bacteria are exposed to penicillin?
Penicillin lyses the bacterial walls.
You see a decline in bacterial growth when administering drugs A and B. When drug A is removed, bacterial growth remains stagnant. When drug B is removed bacterial growth resumes. What type of antibiotics are drugs A and B?
Drug B is a acteriostatic antibiotic and it inhibits cell growth. Drug A is a bactericidal and it kills the microbe.
How does a lab use plate dilution to test the minimal inhibitory concentration (MIC)?
Add antibiotics until 99% of the bacteria are killed from the plate
How does a lab use tube dilution to test the minimal lethal dose (MLD) of an antibiotic?
Bacteria is added to a tube of antibiotic of X concentration and watched to see if it grows.
How do you use disc diffusion method to test which drug would be good for a particular bacteria?
Add the antibiotic disc and look to see if it inhibits growth.
When considering combining antibiotics, you find that the combination is just as good as a single antibiotic. What is this called?
When considering combining antibiotics, you find that the combination is equal to the sum of both antibiotics' effects. What is this called?
When considering combining antibiotics, you find that the combination completely clears the infection better than any single one could've done. What is this called?
When considering adding a bactericidal and bacteriostatic drug, you find that effect of the bactericidal is diminished because it targets cell wall synthesis and the bacteriostatic drug prohibits replication of the cell. What is this called?
Why must you take special consideration when a patient wants an antibiotic for an abscess or necrotic tissue?
Blood flow is decreased to that area and oral antibiotic will have a hard time getting there.
What ways are microbes resistant to antibiotics?
Intrinsically, acquired spontaneously and R plasmid transfer
How did MRSA and MDTB become so rampant in the last decade?
Selective pressure from overprescribing of antibiotics
You prescribe sulfa antibiotics to a patient with a bacterial infection. By prescribing this, what assumption are you making about the bacteria's metabolism?
You assume that it needs and makes its own folic acid because sulfa drugs only work if they can target dihydropteroate synthetase in bacterial folic acid synthesis as competitive inhibitors for the enzyme.
Why is Trimethoprim a good synergistic drug for sulfa drugs?
It inhibits folic acid production further down the pathway so that intermediates already in the cell cannot be used for synthesis.
How do Rifampin and Rifabutin work as antibiotics?
They bind to the beta-subunit of RNA polymerase and inhibit transcriptional initiation. These work for Gram +, Neisseria and Mycobacteria. Eukaryotic structural differences make it selectively toxic.
What type of antibiotics target DNA replication?
Quinolones. They target DNA topoisomerase II and thus replication.
Metronidizole completely disrupts DNA structure, tearing it to pieces. Our DNA is similar to bacterial DNA, so how is it selectively toxic?
It is a pro-drug, meaning it must be metabolized before it becomes active. We do not have the enzymes to metabolize it and thus our cells remain unharmed.