Antibioticresistancecasestudyworksheet

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Dec 6, 2023

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NATIONAL CENTER FOR CASE STUDY TEACHING IN SCIENCE Antibiotic Resistance: Can We Ever Win? By Maureen Leonard, Biology Department, Mount Mary College, Milwaukee, WI Part I – Measuring Resistance Exercise 1 Plate S. aureus MRSA 1 PE 15 mm 0 mm ME 6 mm 0 mm CE 12 mm 0 mm VA 9 mm 13mm 2 PE 14 mm 0 mm ME 11 mm 0 mm CE 14 mm 0 mm VA 11 mm 12 mm 3 PE 18 mm 0 mm ME 8.5 mm 0 mm CE 20 mm 0 mm VA 6 mm 9 mm Exercise 2 S. aureus MRSA Average SE Average PE 15.7 1.2 0 ME 8.5 1.45 0 CE 15.3 2.4 0 VA 8.67 1.46 11.3 Exercise 3 Redraw Table 1 and 2 into a single, more organized table. Be sure to label the table appropriately. Exercise 4 Graph the results from Table 2. Be sure to label the figure and axes correctly.
Answer the following questions Questions 1. What do you think the experimental question is? I think the experimental question is which antibiotic is more effective against staph & MRSA. 2. What hypotheses can you come up with to answer the experimental question? a hypothesis that I can come up with to answer the experimental question would be penicillin penicillin would be the most effective antibiotic staph. while Vancomycin will be the most effective against MRSA. 3. If your hypothesis is correct, what would the plates look like (i.e., what predictions would you make for each hypothesis)? The plates for staphylococcus aureus would have the largest inhibition zones around penicillin, and the plates for MRSA would have the largest inhibition zone around vancomycin. 4. Is the experiment you just collected data for an appropriate test of the experimental question you came up with in your answer to Question 1? 5. Which antibiotics where most effective against S. aureus? Against MRSA? penicillin and vancomycin 6. When comparing the antibiotics effective against both, were there differences in effectiveness? Yes, there’s effectiveness was different, MRSA demonstrated resistance to the most effective antibiotic against Aureus 7. What other questions do the data shown in Figure 1 make you think of? Why is penicillin more effective? Part II – Resistance Questions
1. Describe what is happening in Figures 7 and 8 in a complete sentence of your own words. 1. The lactam antibiotic shown in 7 binding the active site and blocking the formation of cross bridges . Figure 8 shows how vancomycin inhibits the development of cross bridges by preventing PBPS from attaching to the protein sequence. 2. What are the differences in how -lactam antibiotics and vancomycin work? The difference in how lactam antibiotics and vancomycin works is that vancomycin binds directly to the cell wall, while beta lactam antibiotic binds to thepen protein. 3. What other mechanisms might arise to allow resistance to the -lactam antibiotics? Another mechanism that may arise to allow resistance to the lactam antibiotics is bacteria can develop genetic mutations to resist against B lactam antibiotics 4. Could resistance arise to vancomycin? Why or why not? Yes, resistance could arise from vancomycin because antibiotics can develop resistance strains. This is due to mutations in the bacterial genome that could trigger structural changes in the antibiotic, rendering it to be ineffective. Part III – Restoring Susceptibility Questions 1. What do you think the experimental question is? How long each bacterial specimen will survive after being treated with antibiotics 2. What hypotheses can you come up with to answer the experimental question? 3. What predictions would you make for each hypothesis? 4. Looking at the data in Table 1, what do these numbers mean? (Keep in mind a log value means each integer increase is actually a ten-fold increase in the number of cells.) The numbers show that FtsZ inhibitors imipenem and MRSA growth in mice by reducing CFU numbers by 20 or 30 times. 5. What do you think FtsZ inhibitor and imipenem are? FtsZ inhibitor and Imipenem reduces MRSA strain growth, the combination of the two result in much less growth and high antibacterial activity.
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6. Does Table 2 change your interpretation of the experimental data from Question 4? Why or why not? No table number two does not change my interpretation of the experimental data from question four because there is still a large decrease in MRSA cells in those treated with the FTsZ inhibitor and Imipenem combined. 7. How eff ective was the FtsZ inhibitor alone? Imipenem alone? Both FTsZ and Imipenem are not effective alone but when they are used together they can be very effective. 8. How eff ective was the combination of the inhibitor and the -lactam antibiotic? when the inhibitors in the lactam antibiotic are combined and the antibacterial was higher than when used separately. 9. How would you explain these results? The results, so that combining drugs has a greater antibacterial or synergistic impact. 10. What questions would you pursue next?