BIOL 238 Review 2011

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This page provides review questions for BIOL 238 (Spring 2013). Answers may be posted by students.

Chapter 1

[Note: To answer a question in edit mode, please place your answer like this, inbetween two double-line breaks.]

1. What historical discoveries in microbiology, both medical and environmental, laid the foundation for the discovery by Rita Colwell and Anwar Huq of an inexpensive way for Bangladeshi villagers to prevent cholera?

2. The Colwell interview depicts three different ways of visualizing microbes. What are the capabilities and limitations of each method? Which method(s) would have been available before Leeuwenhoek? By Leeuwenhoek? For Peter Mitchell and Jennifer Moyle?

3. Compare the "family tree" of life as drawn by Herbert Copeland, Robert Whittaker, Lynn Margulis, and Carl Woese. How were they similar, and how did they differ? How did their differences relate to different tools available for study?

4. Outline the different contributions to medical microbiology and immunnology of Louis Pasteur, Robert Koch, and Florence Nightingale. What methods and assumptions did they have in common, and how did they differ?

5. Does the human immune system react similarly to both attenuated pathogens and more active pathogens?

6. Outline the different contributions to environmental microbiology of Sergei Winogradsky and Martinus Beijerinck. Why did it take longer for the significance of environmental microbiology to be recognized, as compared with pure-culture microbiology?

7. It is always necessary to prepare a tissue culture to study viruses, as they can't grow without a host cell. Do certain bacteria need tissue in their cultures?

8. How did Alexander Fleming's cultured plate of Staphylococcus become moldy with Penicillium notatum? Is it common for petri dishes to become moldy if left in the open air for too long?

Chapter 2

1. Explain what features of bacteria you can study by: light microscopy; fluorescence microscopy; scanning EM; transmission EM.

2. Explain the difference between detection and resolution. Explain how resolution is increased by magnification; why can't the details be resolved by your unaided eye? Explain why magnification reaches a limit; why can it not go on resolving greater detail?

3. How does refraction enable magnification?

4. Explain why artifacts appear, even with the best lenses. Explain how you can tell the difference between an optical artifact and an actual feature of an image.

5. How can "detection without resolution" be useful in microscopy? Explain specific examples of dark-field observation, and of fluorescence microscopy.

6. Explain how the Gram stain works. What are its capabilities and limitations? How does the Gram stain relate to bacterial phylogeny?

7. If shapes of bacteria are common to many taxonomic groups, including spirochetes which cause Lyme disease as well as others, how accurately can different bacteria be identified just based on shape?

8. Why should we believe scanning probe microscopy (SPM) is accurate? If scientists should be concerned by possible artifacts in EM why wouldn‘t they be concerned about artifacts or even further complications in SPM?

9. When would you use TEM over SEM, or vice versa?

Chapter 3

1. Look up a pathogen of interest. Explain the type of cell membrane, cell wall, and outer membrane if any. Explain how any particular components of the membrane and envelope contribute to pathogenesis.

2. Compare and contrast the structure and functions of the cell and the S-layer.

3. The antibiotic linezolid prevents the 50S ribosome subunit from binding the 30S subunit. If you isolate ribosomes by ultracentrifugation, how might the results in the tube look different with linezolid present?

4. In the laboratory, what selective pressure may cause loss of S-layers over several generations of subculturing? Similarly, why would subcultured bacteria lose flagella?

5. For one of your card pathogens, explain what specialized structures it has, such as pili or storage granules. Explain how they might contribute to pathogenesis.

6. Why might a human cell have a protein complex that imports a bacterial toxin? How might such a situation evolve?

7. What aspects of the outer membrane prevent phagocytosis, and how?

8. If the peptidoglycan cell wall is a single molecule, how does the cell expand and come apart to form two daughter cells?

9. Explain two different ways that an aquatic phototroph might remain close to the light, or that an aerobe might remain close to the air surface.

Chapter 4

1. Suppose in Yellowstone Park, Mammoth Spring, a thermophilic bacterium (Bacillus steareothermophilus increases its population size by ten-fold in 40 minutes. What is the generation time, or doubling time? Why might these bacteria grow faster than Bacillus megaterium, in our laboratory at Kenyon?

2. Mycobacterium tuberculosis, the cause of tuberculosis (TB), has a generation time of 18 hours. How many days will it take to grow a colony containing a million cells? What is the consequence for research on TB?

3. Explain the different mechanisms that membrane protein complexes can use to transport nutrients: ABC transporters, group translocation, and ion cotransport (symport and antiport). Discuss the advantages and limitations of each mechanism.

4. Under what growth conditions do bacteria eat the contents of other bacteria? How do they manage do do this? What is the significance for medical research?

5. In the laboratory, why is it important to grow isolated colonies? What can occur in colonies that we might not notice? What research problems cannot be addressed with isolated colonies?

6. Compare and contrast the advantages and limitations of different responses to starvation: stationary phase; sporulation; and fruiting body formation.

7. How do these growth curves of actual microbes (from the BIOL 239 lab) differ from the textbook "standard"? What might be the cause of the differences, and the relative advantages and limitations?

Growth curves of different microbial species growing in a pitcher plant.

8. Borrelia burgdorferi, the cause of Lyme disease, has a doubling time of 15 hours. If you inoculate a tube of medium with 1 bacterium, how many days will it take to grow a million bacteria?

9. An imaginary “Andromeda strain” has a doubling time of 2 minutes. If you start with one particle, how many will there be after an hour? Why do you think Hollywood is more likely to show a story about an Andromeda strain than about Borrelia?

Chapter 5

1. Look through a grocery store, inspecting the labels of packaged foods. What chemical preservatives do you recognize, and what is their mechanism for killing bacteria or inhibiting growth? For example, propionate and sorbate are membrane-permeant acids that depress cytoplasmic pH.

2. Explain the major difference between the effects of general sterilization and disinfectants, versus antibiotics such as penicillin or streptomycin. Why do antibiotics rapidly select for resistant strains, whereas disinfectants and sterilizing agents do not?

3. Explain which extreme environmental conditions select for membrane unsaturation. What is the advantage of unsaturated membranes for these conditions?

4. Explain how protein structure is modified during evolutionary adaptation to high temperatures, or to high pressure.

5. Suppose it takes a heat treatment 3 minutes to halve the population of bacteria in the food. How long will it take to decrease the bacteria content by 2D-values? Would you want to eat the food at this point? Explain.

6. What kind of habitats will show halophiles? What is the difference between moderate halophiles, extreme halophiles, and halotolerant organisms? Describe what will happen to halophile populations in a pool under the hot sun.

7. What is the mechanism of killing of organisms by ionizing radiation? Why is ionizing radiation less effective on frozen foods?

Chapters 6 and 11

1. Discuss the different functions of different structural proteins of a virion, such as capsid, nucleocapsid, tegument and envelope proteins. How do these functions compare and contrast with functions of cellular proteins?

2. Explain how viruses are cultured, and how a pure isolate of a virus can be obtained. How do the procedures differ from that of pure culturing bacteria? What special difficulty arises when defining genetically pure isolates of RNA viruses such as herpes and HIV?

3. How can strongly oncogenic viruses be assayed in culture, if they don't produce plaques?

4. What are the relative advantages of the virulent phage life cycle of phage T4; the lysis-lysogeny options of phage lambda; and the slow-release life cycle of phage M13? Under what conditions might each strategy be favored over the others?

5. Compare and contrast the life cycles of Herpes virus and HIV (AIDS). What do they have in common, and how do they differ?

6. RNA viruses and DNA viruses represent fundamentally different reproductive strategies. What are the relative advantages and limitations of each? How do their different strategies impact the immune response, and the development of antiviral agents?

7. Discuss the role of host-modulating viral proteins in in herpes viruses. What various kinds of functions do these proteins serve for the virus; and what are their effects on the host?