Download Reading Guide for Week 11_new

Reading Guide for Week 11 – Bio260
Colleen Sheridan
Stage 03 – Invasion! Immunity and Pathogenesis
Our bacteria have established themselves in our host’s body by adhering and growing through binary fission.
We’ve studied how our body fights back (innate and adaptive immunity). Now let’s look at how bacteria and
viruses counterattack by causing disease (pathogenesis).
In this week’s reading you will learn about:
1. Host-Microbe interactions and pathogenesis
Essential question: As you are reading, keep asking yourself, “How is this helping me to understand how
microbes cause disease?”
Chapter 16: Host-Microbe Interactions (16.3-16.10), plus some reading about different diseases (see
below)
1. What is the difference between colonization and infection?
2. What is the difference between subclinical and infectious disease? What are signs and symptoms?
3. What is the difference between a primary infection and a secondary infection?
4. What is the difference between a primary pathogen and an opportunistic pathogen?
5. What is virulence? What are virulence factors? We will continue to develop this key concept in Stage 03 of
our disease progression timeline when we study immunity and pathogenesis, but start to get a handle on it now.
6. Be able to describe the characteristics of infectious disease such as the infectious dose, the course of disease,
the duration of symptoms, and the distribution of the pathogen.
7. Be able to list Koch’s postulates and understand its importance in establishing the germ theory of disease.
8. Again, in your understanding of what virulence means, understand that Molecular Koch’s postulates allow us
to determine specific microbial genes (or their protein products) that are responsible for the virulence, or how
much disease is produced, of the microbe.
9. Be able to discuss what “distinguishes pathogens from other microbes.”
10. Review “Mechanisms of pathogenesis” on pg 385 and describe each of the following and give an example:
a. Production of toxins that are then ingested
b. Colonization of mucous membranes on the host, followed by toxin production
c. Invasion of host tissues
d. Invasion of host tissues, followed by toxin production
11. What makes a successful pathogen?
12. Does adherence alone determine whether a microbe will cause disease? Why?
13. Be able to describe the “requirements of adherence and colonization,” and the importance of cellular
structures for this to happen. Brain teaser: Do you remember why is iron so important to a cell?
14. Understand how another Gram-negative cellular structure, the type III secretion system, can help to
establish microbial infection.
**The chapter is organized to inform you about how bacteria 1) colonize the surfaces of a host or 2) invade host
tissues, and 3) how bacteria evade our immune responses while doing so. Then it discusses how damage to the
host happens as a result of 4) bacterial toxins or 5) our very own immune response! It then discusses how 6)
viral and 7) eukaryotic pathogens cause disease.
16.6 - Invasion
15. Why might it be beneficial for microbes to invade across the epithelial barrier?
16. How can microbes penetrate the skin? Know how Staph. aureus gets in.
17. How can microbes penetrate mucous membranes? What is a Type III secretion system? Know how
Salmonella, Shigella and M. tuberculosis get in.
16.7 – Avoiding Host Defenses
Hiding in a host cell
18. What parts of the immune system do bacteria hide from while inside a host cell?
19. What type of immunity (humoral or cell-mediated) needs to be activated to get rid of bacteria hiding inside
host cells?
20. Knowing that it takes 1-2 weeks for an efficient primary adaptive immune response to get going, do you
think that hiding inside of host cells is a good strategy? Why/why not?
Avoiding Destruction by Complement
21. Remind yourself of the three primary outcomes of activation of complement (pg 344).
22. Why do MACs affect Gram (-) cells and not Gram (+) cells?
23. Serum is the fluid part of blood without any clotting factors in it. Still contained within the serum are other
blood proteins, complement proteins. and antibodies. What does it mean to be “serum resistant” and what
method do Neisseria gonorrhoeae (pronounce “eae” as “ee-ee”) use?
Avoiding Destruction by Phagocytosis
24. Remind yourself of the many steps involved in phagocytosis (pg 347). Describe the various mechanisms
used by bacteria to avoid destruction by phagocytosis:
a. Preventing encounters: list them out and describe them (know how S. pyogenes uses this method)
Application: What type of hemolysis does S. pyogenes produce on blood agar plates? What
causes this hemolysis? From your lab manual, is hemolysis always associated with disease?
b. Avoiding recognition and attachment: list them out and describe them (know how Streptococcus
pneumoniae (“iae” = “ee-ee”), Streptococcus pyogenes, and Staphylococcus aureus use this
method)
c. Surviving within phagocytes: list them out and describe them
 what advantages are available to bacteria that hide inside macrophages?
(know how Listeria, Shigella, Salmonella, and Coxiella burnetii (“ii” = “ee-ee”) survive)
 Look up Tuberculosis (pg 502) and read about Signs and Symptoms, Causative Agent,
Pathogenesis, and Epidemiology. We’ll get to Treatment and Prevention when we start learning
about antibiotics.)
Avoiding Antibodies
25. Remind yourself of the many protective outcomes that antibodies have (pg 361). How can microbes avoid
antibodies? List them out and describe them (Know how N. gonorrhoeae and S. pyogenes do this)
26. Read pg 178: Natural Selection. Describe how antigenic variation works at the level of gene expression in
N. gonorrhoeae).
16.8 – Damage to the Host
27. What causes direct damage to the host during an infection? What causes indirect damage?
28. How could a pathogen benefit from causing damage to the host?
Exotoxins
29. What is an extotoxin? Is it a protein? How is it produced? What types of bacteria produce them?
Generally, what do they do? How are they released? Where do they act?
30. Why is vaccination so important when talking about exotoxins? What is a toxoid?
31. What are neurotoxins, enterotoxins, and cytotoxins?
32. Be able to describe the mechanisms of action of A-B toxins, membrane-damaging toxins, and superantigens.
33. I really like this question in the book when describing A-B toxins, “Would an antibody response against the
B subunit protect against the effects of the toxin?” p.393
34. From Table 16.1 pick 2 A-B toxins, 1 membrane-damaging toxin, and 1 superantigen and learn more about
how they work by researching them on their “Page Reference” in the book. For the exam be able to name the
toxin, the bacterium that makes it, the characteristics of the disease, and draw a labeled diagram with an
explanation of how they work.
35. Often the damage helps the bacteria to leave from the portal of exit. Does the mechanism of action of your
chosen exotoxins help in this way? If so how? If not, what other benefits to the bacterium might this damage
provide?
36. What is “pus”? Look it up in the glossary in the back of the book. Why do you think some membranedamaging toxins would cause an accumulation of pus?
Endotoxin and Other Bacterial Cell Wall Components
37. Why do you think it might be beneficial for our innate immune cells to recognize conserved structural
components of bacteria?
38. What is endotoxin? Remind yourself of the structure of LPS (pg 61).
39. Be able to compare endotoxin with exotoxin (Table 16.2)
40. Compare the immune response to localized endotoxin versus systemic endotoxin.
41. Read about sepsis and septic shock (p 674) as it is considered a healthcare-associated disease. What are the
causative agents? Describe the pathogenesis.
42. How is LPS detected by the immune system and what is the response?
43. Know that other bacterial cell wall components can also lead to septic shock.
Damaging Effects of the Immune System
44. How can inflammation cause damage? Read about Neisseria gonorrhoeae (p 622). N. gonorrhoeae is now
frequently antibiotic resistant! Describe the causative agent and its pathogenesis.
45. How can the adaptive immune system cause damage? Read about S. pyogenes (p.487). Describe the
causative agent and its pathogenesis.
16.9 – Mechanisms of Viral Pathogenesis
46. What must a virus do to infect a host? Describe the process. What is the receptor for HIV? Which cells
express this receptor? Describe how poliovirus can cause brain and spinal cord infection when it initially infects
the digestive tract.
47. How can viruses avoid the effects of interferons?
48. Describe how viruses can regulate host cell death.
49. Describe how viruses can avoid antibodies. What a minute! Aren’t viruses obligate intracellular parasites
that activate cell-mediated immunity? How can they activate humoral immunity to make antibodies? Think
about the viral life cycle. Are viruses ever found outside of cells?
16.10 – Mechanisms of Eukaryotic Pathogenesis
50. What disease does Plasmodium vivax cause? The other most common cause of this disease is Plasmodium
falciparum. How does it attach to host cells? How can some people be resistant to P. vivax infection? How
does Plasmodium gain entry to red blood cells? Why is it beneficial to this eukaryotic parasite to infect red
blood cells?
51. Malaria is the number one infectious disease killer in the world, followed by tuberculosis and HIV. Read
about malaria (p. 686). Describe the causative agent and its pathogenesis.