Short Answer Questions for Exam 3, Biology 250

1. What characteristics should an antigen have to stimulate an immune response effectively?
2. Briefly, what do each of the following do in an immune response? macrophage, helper T lymphocyte, cytotoxic T lymphocyte, delayed hypersensitivity T lymphocyte, suppressor T lymphocyte, B lymphocyte, plasma cell
3. Where do all these (prededing question) cells come from?
4. In what parts of the body do immune responses happen?
5. What cells are involved in the interaction that results in antibody production? For what is the antibody that is made specific?
6. What is antibody? Where is it made, by what cells, where is it located after it is made, what use is it?
7. What is antigen?
8. What is meant by immunological memory? What really happens to cause it? What are the differences between a primary and a secondary response?
9. Distinguish between antibody specificity and classes of antibody molecules.
10. Each antibody class has several (3-4) unique features that distinguish it from the others, in terms of structure, function or both. What are they? (For our purposes, the classes are IgM, IgG, IgA, and IgE.)
11. What and where are antigen binding sites on antibody molecules?
12. Describe how a person allergic to oak pollen might begin to suffer from the symptoms of hay fever. That is, the person inhales the pollen. Then what? How is IgE involved? Mast cells?
13. Why does it make sense to treat IgE-mediated allergies with antihistamines? Would it make sense to treat poison ivy with antihistamines?
14. Why are drug and venom allergies likely to have so much more serious consequences than hay fevers? What are the consequences?
15. Desensitization shots given to minimize allergies deliver small amounts of antigen on a regular schedule. Give two possible explanations for how they work.
16. How do antibodies act indirectly to lead to the elimination of antigen by other parts of the immune system?
17. In what cases do antibodies have a direct effect that inactivates certain antigens?
18. Against what targets are cytotoxic T cells an effective defense? What cells cooperate to activate cytotoxic T cells? What happens to the target cell?
19. How do delayed hypersensitivity T lymphocytes participate in allergic reactions to antigens like those of poison ivy or tuberculin?
20. Why is it incorrect to say that people who do not exhibit a skin reaction in a positive tuberculin skin test or a poison ivy rash are immune to the allergen?
21. Discuss various examples of nontoxic virulence factors. How are they important to the pathogen's survival?
22. Distinguish between endotoxin and exotoxins. (Look for eight differences!) Why is one singular and one plural in the first sentence in this question?
23. Discuss the range of importance that a toxin may have in causing the symptoms of a disease, giving examples.
24. Compare the progress of an infectious disease through a well-immunized population with its progress through a poorly immunized population.
25. What substances are involved in invasion and colonization by Streptococcus pyogenes? What does each of these substances do?
26. What is the significance of an anti-SLO titer? Give three examples of suppurative types of Streptococcus pyogenes infection.
27. What streptococcal disease requires virus infection of the bacteria?
28. Explain how a person might develop rheumatic fever and its relationship to streptococcal disease. Why would treating streptococcal infections with antibiotics prevent rheumatic fever?
29. Give two other examples of nonsuppurative complications of streptococcal infection.
30. What effect does diphtheria toxin have on host cells? What happens to the host as a result?
31. What is a pseudomembrane and what does it have to do with diphtheria?
32. Name five kinds of bacteria that cause lower respiratory tract disease.
33. What is the most significant factor in the ability of Streptococcus pneumoniae to cause disease?
34. What bacterial substance helps pathogenic Streptococcus pneumoniae resist host defenses?
35. Why are the very young and the very old particularly vulnerable to Streptococcus pneumoniae?
36. What makes Mycobacterium tuberculosis acid-fast?
37. How is this (preceding question) related to its ability to cause disease?
38. What single factor is the most important in the pathogenesis of Mycobacterium tuberculosis?
39. What are four possible results of primary infection by Mycobacterium tuberculosis?
40. How does the development of cell-mediated immunity by the host change the character of the disease/lesions in tuberculosis?
41. What is reactivation infection in tuberculosis?
42. How is tuberculosis diagnosed and treated?
43. How are organisms that cause GI tract disease usually transmitted?
44. Give three examples of bacteria that cause food poisoning due to bacterial toxins and three examples of bacteria that cause food poisoning by colonizing the GI tract.
45. Trace the process by which Clostridium botulinum causes botulism without invading or colonizing the host. (spores, germination, vegetative cells, toxin, toxic effects, etc.)
46. What conditions are required for germination of Clostridium botulinum spores? Where might you find such conditions? Could they ever exist in the human body?
47. Describe a scenario for food poisoning by Salmonella typhimurium? What accounts for most of the symptoms in this type of food poisoning?
48. Why is this type of food poisoning not necessarily treated with antibiotics?
49. What two characteristics of Salmonella typhi are most important in its ability to cause disease?
50. How is endotoxin involved in typhoid fever?
51. Describe the three phases of typhoid fever? Where are the bacteria located in each phase?
52. How is cell-mediated immunity involved in typhoid fever?
53. In what diseases are carriers important and what role do they play in transmission of the disease?
54. How can GI tract diseases like typhoid fever, bacillary dysentery, and cholera be prevented and controlled?
55. What toxins are involved in causing bacillary dysentery? Describe the course of the disease.
56. How does the colonization of the host by Shigella dysenteriae differ from that by Salmonella typhi?
57. How is Vibrio cholerae transmitted between hosts?
58. What effect does choleragen have on host cells in the intestinal tract?
59. How does colonization of the host by Vibrio cholerae differ from that by Salmonella typhi and Shigella dysenteriae?
60. How is cholera treated and why is this form of treatment necessary?
61. Which of the organisms that we have talked about grows intracellularly? In what host cells?
62. Which of the organisms that we have talked about causes disease due to its production of a potent exotoxin?
63. What role do CFA-I and CFA-II play in the pathogenesis of enteropathogenic Escherichia coli? The LT and ST toxins? Which is similar to choleragen? How are these virulence factors related to the symptoms? What characteristics place patients at the greatest risk for disease due to enteropathogenic E. coli?
64. Make a giant table with the pathogens discussed in class across the top and the various aspects of pathogenesis (characteristics of organism, transmission, invasion, colonization, virulence factors, complications, course of disease, symptoms, diagnosis, treatment, epidemiological concerns, misc.) down the side. STUDY IT!!