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- Explain the role of pylori in the pathogenesis of peptic ulcers. Which populations are most susceptible to peptic ulcers? Is H. pylori normal flora? If so, what causes the species to become pathogenic? Construct at table to compare and contrast the 5 steps of microbial pathogenesis. How does extracellular growth differ from intracellular growth? Diagram the 5 step pathogenesis cycle for coli O157:H7, an extracellular, intestinal pathogen acquired by consuming contaminated food/water. Be sure to include the role of exoenzymes and the Shiga exotoxin in your diagram. (2 points) Explain the pathogenesis of Listeria monocytogenes. Be sure to include temperature regulation, intracellular growth, and at risk groups in your discussion.Compare the mechanism of virulence for Vibrio cholerae and enterotoxigenic E.coli. Specifically, how do these bacteria bind to host cells and what factors are involved in producing the diarrhea observed in infected patients?Before development of a vaccine against this microbe, thedisease it caused accounted for two-thirds of bacterial meningi-tis cases during the first year of life but is still the number oneleading cause of mental retardation in patients who survive seri-ous disease due to permanent central nervous system disorders.What is the microorganism?(a) Haemophilus influenzae type B(b) Haemophilus influenzae type A(c) Neisseria meningitidis(d) Streptococcus pneumoniae(e) Listeria monocytogenes
- While it is true that not all coliforms are pathogenic under normal conditions, please name two situations that can occur due to infection by pathogenic strains.What are the common pathogens isolated from stool samples? What is the difference between a coliform bacterium and a noncoliform enteric bacterium? What diagnostic test differentiates Proteus and Providencia species from other Enterobacteriaceae? How would you differentiate between serotypes of E. coli? Are the gram-negative enteric bacilli fastidious organisms? Would they survive well outside of the body? If so, what significance would this have in their transmission? Why is serotyping particularly important in Salmonella infections and typhoid fever?Approximately 50% of the world’s population is colonised by Helicobacter pylori (H. pylori), yet only a fraction of the population develops gastric ulcers. A. Why is there a discrepancy between the frequency of H. pylori colonization and the frequency of gastric ulceration? Is H. pylori colonization responsible for gastric ulcers? B. Should a vaccine against H. pylori be developed and administered for everyone? Justify your reasoning.
- What virulence factor, present in Streptococcuspneumoniae but absent from Salmonella enterica, makesS. pneumoniae so highly virulent for mice?What are the treatment approach of H.pylori infection after failed the initial therapy? Please briefly explain at your own words.What does the term nosocomial infection mean? What is the difference between an endogenous nosocomial infection and exogenous nosocomial infection? Describe the various infections produced by Pseudomonas aeruginosa .
- Below are a list of virulence factors/ strategies paired with an example of an organism that utilizes them. How do each of the following strategies contribute to the virulence of the pathogen? Strategy - Causes the host to produce more receptors (Organism - Rhinovirus) Strategy - Produces gas as a product of fermentation (Organism - Clostridium perfringens) Strategy - Produces a capsule (organism - Klebsiella pneumonia) Strategy - Ability to move between adjacent cells (organism - Cytomegalovirus) Strategy - Ability to use pilus as a motility structure (organism - Pseudomonas aerogenosa)The general public takes for granted the link between an infectious agent and a given infection Discuss the requirements established by Koch, the nineteenth-century German scientist, before ascertaining, for instance, that Helicobacter pylori bacterium is the cause of the gastric ulcer. Why is it so essential to meet these conditions?Name the metabolic end products that can facilitate the spread ofstreptococci and initiate secondary sites of streptococcal infection.