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Bact. 303 Study Questions V

University of Wisconsin - Madison

Host-Parasite Interactions


146. In bacterial-animal symbioses, what is the distinction between mutualism and commensalism? What is parasitism? What is the difference between a parasite and a pathogen? What is an opportunistic pathogen? What is endogenous bacterial disease? What sorts of bacteria are involved in endogenous diseases? What are the conditions which "cause" endogenous disease?

147. What is meant by the term normal flora of a plant or animal?

148. What are "germ-free" animals? How are they obtained and maintained? Describe some of the types of experiments that have been done with germ-free animals that contribute to our knowledge of nutrition and physiology of animals, infectious diseases, and microbial ecology.

149. What are the predominant bacteria on the various surfaces of the human body? How are these indigenous bacteria or normal flora beneficial to their host? How may they be harmful? Name some ways bacteria on body surfaces can antagonize one another. How can they "cross feed" one another?

150. What role do indigenous microflora play in dental caries? What specific types of bacteria are thought to be involved? How can regular flossing and brushing of the teeth and reduction of dietary sucrose decrease cariogenesis?

151. What is virulence of a pathogen? What are the main factors that contribute to the pathogenicity (virulence) of a microorganism?

152. What kinds of bacterial surface structures or molecules, in this case called adhesins, are involved in specific adherence of pathogens and are required to initiate infection. Give examples of bacteria that require specific adhesins in order to colonize their respective hosts.

153. Discuss the mode of action of these bacterial substances and how each might aid a pathogen in its invasion of the host: hyaluronidase, streptokinase, coagulase, leukocidin, collagenase, hemolysin.

154. What kinds of bacterial surface structures are involved in the resistance of pathogens to engulfment and/or killing by phagocytes? Give examples of how specific bacteria are resistant to phagocytosis.

155. Compare and contrast the properties of bacterial exotoxins and endotoxins. What are enterotoxins? Are they most like exotoxins or endotoxins? Explain.

156. Among the bacterial protein toxins that have an "A+B subunit arrangement", explain the separate functions of the A subunit and the B subunit.

157. What is the general mode of action of the following toxins: salmonella endotoxin, diphtheria toxin, botulinum toxin, tetanus toxin, cholera enterotoxin, pertussis toxin?

158. Distinguish between food-borne infections and intoxications, and identify some of the major bacteria involved in each type of food poisoning.

159. Illustrate and describe in detail the lipopolysaccharide component of the salmonella cell wall which constitutes endotoxin. What portion of the LPS is toxic? What portion is antigenic? What are the effects of endotoxin in an animal?

160. What factors are considered to be the constitutive (natural) defense mechanisms of a host against pathogenic microorganisms? Name several examples of anatomical, chemical, cellular or microbial defenses against pathogens considered innate or natural.

161. If a pathogen breaches the surface of the body, what types of cellular defenses will come into play for the host? Consider this to mean both constitutive (natural) and inducible (immune) defenses that are mediated directly by cells or their products.

162. How do phagocytes slow or eliminate invasion by pathogens? What are the steps in the phagocytic process that lead to ingestion and destruction of pathogens? How do bacteria that are intracellular pathogens of macrophages or other phagocytes avoid being destroyed by their host cells?

163. Many types of cells in the body play a role in defense. Which types of cells in the body are involved in inflammation, phagocytosis, immediate hypersensitivity, delayed hypersensitivity, cell-mediated immunity and antibody production?

164. What is inflammation? How is the inflammatory response beneficial to the host? How is it harmful? How are bradykinin, complement and histamine involved in inflammation?

165. What is meant by immunity of a host to a pathogen? Differentiate between natural and acquired immunity. Differentiate between active and passive immunity and name two ways to acquire each.

166. What is the classic definition of an antigen? Give some examples of antigens. What is an antigenic determinant? What properties must a substance have to be antigenic?

167. What are antibodies? What are the general physical and chemical properties of antibodies? Describe and differentiate the classes of immunoglobulins. What are the specific functions and biological properties of each type of immunoglobulin?

168. Why does an infant usually have immunity to a number of diseases just after birth but become more susceptible later?

169. Describe several types of antigen-antibody reactions that would be useful to the host in resistance or elimination of a specific pathogen.

170. What is complement? Explain the role of complement in killing of bacterial cells in the presence of specific antibody. How does complement increase the efficiency of phagocytosis?

171. How will antibody titer (concentration in an animal) change after one injection of an antigen? After a second injection? How could an antigen-antibody reaction be useful in the diagnosis of a disease?

172. Describe the overall process of antibody production when an antigen is encountered for the first time by the immunological (lymphatic) system: discuss the involvement of macrophages, B-lymphocytes, plasma cells, T-lymphocytes. Interleukin (IL)-1, IL-2, and IL-4. What are "memory cells"? What is their role in a secondary, (memory) response to a second encounter with antigen?

173. Exactly what are the properties of and differences between T-lymphocytes and B-lymphocytes?

174. What is the difference between antibody-mediated immunity (AMI) and cell-mediated immunity (CMI)? Which type of immunity is most important against bacterial infections? Against virus infections? Explain.

175. Name several classes of effector T-lymphocytes which develop following antigenic stimulation. What are some of the functions and activities of these T-cell populations (TC, TDTH, TH1,TH2 etc.) during the cellular immune response?

176. What is the relationship between the HIV virus which causes AIDS and specific T-lymphocytes that results in immunodeficiency.

177. What is interferon? During what sorts of infections is interferon an important part of the resistance complex? How does the action of interferon differ from the action of antibody as a defense against viruses?

178. What are the causes, manifestations and mechanisms of atopic allergy? How is IgE involved in atopic allergy? What is anaphylaxis? How can an individual become desensitized to a substance which elicits an atopic allergic response?

179. What is delayed hypersensitivity and how is it different from immediate hypersensitivity? Are antigens involved? Are antibodies involved? What is the role of T-lymphocytes and macrophages in the delayed hypersensitive response? Is there a memory response? What is the role of lymphokines? What are some examples of delayed hypersensitivity?

180. Define each of the following terms: vaccine, toxoid, booster, titer, attenuation, antitoxin, antiserum, hyperimmune serum, memory response.

181. What is the nature and method of preparation of each of the following vaccines: diphtheria, tetanus, tuberculosis, typhoid fever, whooping cough, German measles, mumps, measles, poliomyelitis, smallpox, influenza.

182. Identify these vaccines: BCG, OP, MMR, DPT.



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Edited with Frontier Applications on a Macintosh on Fri, Mar 14, 1997 at 9:16:52 AM by Kenneth Todar University of Wisconsin-Madison Department of Bacteriology.