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10 thoughts on “D17a – Sees”
Can you elaborate on what it means to be bacteriostatic and why you would want to inhibit bacterial growth rather than kill it.
Yes! Bacteriostatic means that the bacteria is simply inhibited from growing and reproducing due to the drug. The opposite would be bactericidal, which means that the bacteria would be killed by the drug. Both are viewed in the same effectiveness!
Really nice presentation, Emma! I really liked your pink/purple theme! I was hoping you could elaborate more on why DMSO was chosen as a negative control! Thank you!
Yes! We chose DMSO as our negative control because our compound, Melittin, was soluble in it, which made for a much easier time diluting it, as well as being able to accurately accumulate absorbance values from our testing of our well plates in the spectrophotometer over multiple trials of multiple tests. We also previously had a lot of data from DMSO and experience using DMSO, so we knew how to work with it effectively and efficiently, and it ultimately was what we chose to use!
Speaking genetically, by analysing the DNA, how can you tell if an antibiotic is bacteriostatic or bacteriocidal? Does it have to do with epigenetics, like repressor sequences? How do the figures relate to the results?
From a data approach, the definition of a bactericidal agent would be an antibiotic where the ratio of the Minimum Inhibitory Concentration (MIC) and Minimum Bactericidal Concentration (MBC) is less than or equal to 4. Subsequently, the definition of a bacteriostatic agent would be an antibiotic where the ratio of the Minimum Inhibitory Concentration (MIC) and Minimum Bactericidal Concentration (MBC) is greater than 4.
I think you said that melittin is bacteriostatic since it mimics the absorbance of ampicillin. Ampicillin is bactericidal, in hindsight would you change your conclusion to bactericidal?
No, our data indicated that Melittin was bacteriostatic. Our hypothesis was that Melittin would act in a similar fashion to Ampicillin since that was the positive control we chose to use, so our hypothesis was off in that regard, but the data leaned towards being bacteriostatic!
Why do you think the 1:2 dilutions resulted in scattered data whereas the 1:10 dilution provided clear data?
Our 1:2 dilutions weren’t providing a great enough change in concentration of Melittin to show in detail how effective Melittin was or was not against S. Typhimurium, so we switched to the 1:10 model in order to be able to see a more vast range of concentrations: rather than going from 10% to 5% to 2.5% concentration, we went from 10% to 1% to 0.1%, and that made it easier to see at what concentrations our compound was actually effective at!