Payal PatelBiology 140 Section 16Amanda McClellandLab Communication 1The most effective antibiotic on strain C E.ColiIntroductionI learned from the readings that antibiotic resistance is not something that the bacteria consciously do. Resistance is created through mutations and genetic differences that are replicated and produced from the initial surviving bacteria. Many strains of antibiotic resistant Tuberculosis are present today because people who start the antibiotic regimen, many times do not finish them because of its high cost and time commitment. Because of this, a few of the bacteria that survive the beginning rounds of antibiotics because of resistance replicate and create new colonies that are harder to combat than the earlier strain. Tuberculosis is still prevalent today and not just in the poorer regions of the world,but also in the United States. This is why it is important for us to analyze resistance in bacteria (Barry and Cheung 62-64).To experiment and observe resistance bacteria have to antibiotics, we experimented with a nonpathogenic E. Coli strain C. We hypothesized that if strain C is a wild type E. Coli (without transferases), it will be susceptible to the aminoglycosides (Tubramycin, Kanamycin, and Amikacin) because they disrupt protein synthesis. We predicted that if strain C is a wild-type strain, the aminoglycosides will be effective.MethodsIn our group, the materials we used were 4 agar plates, sharpie, tape, strain C E.Coli, swabs, rubbing alcohol, forceps, antibiotic disks, and blank disks. To begin, we split each plate into an equal four parts with a sharpie and labeled what disk we would place on each section (one being a blank disk control). We then swabbed a lawn of strain C E.Coli onto each plate. In the middle of each section a disk was placed. In the first set of plates (2 replicates), ciprofloxacin, Amikacin, and kanamycin antibiotic disks were placed in themiddle of ¾ sections (one on each section). On the fourth section, a blank control disk was placed. On the second set of plates, tobramycin, triple sulfa, tetracycline, and a blankdisk were plated in the same fashion. The plates were stored upside down in the incubatorfor 48 hours at 37 degrees Celsius. Our independent variable was the antibiotic disks we put on the plates. The dependent variable is the zone of inhibition created by placing the antibiotic disks. The four blank disks and the incubation method were the controls. We had two replicates of each antibiotic.The next week, we measured the zone of inhibition for each of the antibiotic disks. To measure, we used a ruler and measured the diameter of the circles in mm. If the zone of inhibitions overlapped, we simply would measure the radius and double the value. We found that triple sulfa had the biggest zone of inhibition, and strain C was susceptible to all of the antibiotics except Kanamycin to which it was intermediate. For strain C, the average zone of inhibition (in mm) for each antibiotic is as follows: amikacin at 26.5, ciprofloxacin at 29.5, kanamycin at 27, tetracycline at 26.5, triple sulfa at 31.5, and tobramycin at 22.5.DiscussionBased on our results, we were able to reject our hypothesis because strain C E.Coli was not susceptible, but was intermediate in resistance to Kanamycin whereas was susceptibleto the other aminoglycosides.From compilation of class results, we learned that different strains of bacteria were susceptible and resistant to different antibiotics. The genetic differences were illustrated by the transferases put into the different strains. Our individual group results explained that one class of antibiotics did not have the same susceptibility (kanamycin vs. Amikacinand tobramycin). We think that the decreased susceptibility to the antibiotic class aminoglycosides as a whole meant that our strain had transferases present. To further investigate, I would want to use a broader range of antibiotics and see how susceptibility would relate to a particular transferase. I would use more replicates, because with only two replicates, there was no room for error, and one mistake significantly altered the results. 05101520253035Zone of Inhibition for Strain C E. ColiAmikacinCiprofloxacinKanamycinTetracyclineTriple SulfaTubramycinZone of Inhibition (mm)AmikacinCiprofloxacinKanamycinTetracyclineTripleSulfaTobramycinReplicate 1 25 44 42 26 33 21Replicate 2 28 15 12 27 30 24Mean 26.5 29.5 27 26.5 31.5 22.5Works CitedBarry III, Clifton E., and Maija S. Cheung. "New Tactics Against Tuberculosis." Scientific American Mar. 2009: 62 -69. Print.Schussler, Elisabeth, Jan Hudson, Erica Rowe, Monique Lemieux, and Sudhir Naswa. Biology 140 Laboratory Manual. Knoxville, TN: General Biology, UTK and Bluedoor, 2012. 1-10. Print.Freeman, Scott. Biological Science. 4thth ed. San Francisco, CA: Pearson, 2011. B19-20.