Where are we heading?

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1 Unit Four: Where are we heading? Outline 2Lesson Unit1.2 Unit 4: Outline Unit 1: What is an infectious disease and why do we care? Unit 2: What does it mean to have an infectious disease? Unit 3: When does a microbe become pathogenic? Unit 4: How do pathogens make us sick? Unit 5: How do we get better? In the previous unit we focused on adaptations and situations that contribute to microbes being pathogenic. This allowed the students to interact with some of the ambiguities associated with defining a microbe as a pathogen. In this unit we turn our focus to how pathogens cause disease. As we will see, two main forces contribute to the feeling of sickness: The pathogen damages host cells via the immune response, or directly, impacting tissue functions and thus causing symptoms. The immune response senses the infection or damage to the host and produces chemicals (cytokines) that result in all the classic symptoms of illness, including fever and pain. How this immune response is generated will not be discussed here it is a focus of the next module. 1

2 Outline Outline UNIT FOUR Unit 4: How do pathogens make us sick? Lesson 1: Why we feel sick how pathogens cause direct and indirect damage This unit introduces the idea that once pathogens gain access to the host they can cause damage. This damage happens for two main reasons: 1) direct damage results from the replication of the microbe or from a toxin the microbe produces. 2) indirect damage results when the immune response attempts to clear the pathogen and self-cells become casualties (this will be further focused on in unit 5). Where the pathogen is located and how fast it replicates also impacts how it damages the host: for instance, intracellular pathogens have different consequences than extracellular pathogens. Lesson 2: Toxins Botox, tetanus, hamburger disease and MRSA This lesson continues to explore how bacteria cause damage to host cells. The last lesson focused on cell damage that results from bacterial replication, this lesson focuses on how bacterial toxins damage the host. Although some toxins damage the host directly, others stimulate immune responses that lead to indirect damage. For example, LPS that is a component of the bacterial cell wall causes damage by activating innate immune cells. It is also important to emphasis that the toxins perform a function for the bacterial life cycle. Lesson 1 Lesson 2 2Lesson Unit1.2 2

3 Outline UNITOutline 2Lesson Unit1.2 FOUR Unit 4: How do pathogens make us sick? Lesson 3: How do bacteria adapt to become pathogens? The adaptation auction. The lessons thus far have emphasized that pathogenic bacteria are microbes that find a way to enter the body and cause damage. This is in contrast to most microbes, which are effectively dealt with by the immune system. So that leaves the question: How do bacteria become pathogenic? This lesson will focus on this question from the perspective of adaptations that give bacteria the ability to bypass different levels of the immune system. Many of the adaptations in the auction activity were introduced in Unit 1. In this activity, the focus should be on further understanding the functions of the adaptations from the perspective of gaining accesses to nutrients and causing host cell damage. In addition, the use of the auction is meant to emphasize that having adaptations cost the bacteria energy which slows growth. Lesson 4: How do viruses make us sick viral replication This lesson extends the principles learned in Unit 4.1 to address how viruses cause host damage. It focuses on how viruses replicate, and then exit from host cells. The lesson also introduces the difference between DNA and RNA viruses and explains that viruses need host proteins to replicate. Furthermore, the virus may damage the host cell during replication, either directly or indirectly, as we saw with intracellular bacteria. The activity introduces the viral life cycle in the context of host cell damage. It was chosen because there are a number of parallels between how viruses cause host cell damage and how intracellular bacteria cause host cell damage. One goal of the discussion is to have students use their knowledge of bacteria-mediated damage to predict how a virus might causes damage. Lesson 4 Lesson 3 Lesson 4 3

4 Outline UNITOutline FOUR Unit 4: How do pathogens make us sick? Lesson 5: How do viruses adapt? antigenic shift and drift and the flu pandemic This lesson extends the principles learned in Unit 4.1 to address how viruses cause host damage. It focuses on how viruses replicate, and then exit from host cells. The lesson also introduces the difference between DNA and RNA viruses and explains that viruses need host proteins to replicate. Furthermore, the virus may damage the host cell during replication, either directly or indirectly, as we saw with intracellular bacteria. The activity introduces the viral life cycle in the context of host cell damage. It was chosen because there are a number of parallels between how viruses cause host cell damage and how intracellular bacteria cause host cell damage. One goal of the discussion is to have students use their knowledge of bacteria-mediated damage to predict how a virus might causes damage. Lesson 6: Designing an antiviral drug the challenge of HIV. This lesson offers students the chance to apply what they have learned thus far to design an anti-viral drug to treat HIV. The video demonstrates a model of how HIV replicates and re-infects a host. The students can use this model to develop their own anti-viral drug targets. The students will then develop their drugs in small groups and prepare to present and defend the logic that they used when designing the drug. Lesson 5 Lesson 6 2Lesson Unit1.2 4

5 Outline UNITOutline FOUR Unit 4: How do pathogens make us sick? Lesson 7: Putting together the strategies pathogens use what kind are you? This lesson gives students an opportunity to exercise their cumulative knowledge about infectious diseases by having them draw parallels between select pathogens in the context of a FACEBOOK quiz. The activity will allow students to work with the information they learned about pathogens. This includes how pathogens spread, where they reside in the host, the requirements for survival of bacteria, viruses, and more. Lesson 7 2Lesson Unit1.2 5

6 Outline OVERVIEW Rationale: This unit introduces the idea that once pathogens gain access to the host they can cause damage. This damage happens for two main reasons: 1) direct damage results from the replication of the microbe or from a toxin the microbe produces. 2) indirect damage results when the immune response attempts to clear the pathogen and self-cells become casualties (this will be further focused on in unit 5). Where the pathogen is located and how fast it replicates also impact how it damages the host: for instance, intracellular pathogens have different consequences than extracellular pathogens. Do Now: The do now has students brainstorm potential mechanisms through which a pathogen causes illness. This leads into a discussion of direct and indirect host cell damage. Lecture/ Socratic Discussion: This activity introduces the concept that a microbe causes damage via lysis of the host cell. This lysis may occur directly or indirectly. The activity then focuses on direct damage via bacterial replication, as illustrated by select pathogens. Wrap Up: The next few lessons focus of specific examples of host damage by pathogens. The wrap-up is intended to reemphasize the important mechanisms of direct and indirect damage that will be seen in the next lessons. Homework: The reading is in preparation for the activity in lesson 2. The Lesson Plan Why we feel sick how pathogens cause direct and indirect damage. 1. Do Now (10 min): Have the students brainstorm: Once microbes get in to the host how do they cause damage? What does it mean that a pathogen directly damages the host? What about indirect damage? 2. Lecture/Discussion (20-25 min): Discussion about direct and indirect damage and how they relate to the location and rate of bacterial growth. 3. Wrap Up (5 min): Recap and reiterate the objectives. 4. Homework: Read an article for the jigsaw activity in lesson 2. 2Lesson1Lesson Unit1.2 Unit4.1 6

7 1. DONOW Have students brainstorm potential mechanisms through which a pathogen causes illness. 2. Lecture and Socratic Discussion This discussion focuses on the two main mechanisms of host cell damage: direct and indirect damage. Ask the students: How do pathogens cause host cell damage? There are two main ways: 1. Direct (caused by bacteria, virus, or parasite). 2. Indirect (caused by immune response to the infection). Ask the students to brainstorm: Once microbes get in how do they make us sick? The main point here is that sickness is what we observe when there is damage to host cells. In the host it is immune cells that sense the invasion and damage and send signals to other immune cells via cytokines that cause fever, redness, swelling, pain, and other symptoms. It is important to emphasize that immune cells induce most feelings of illness because, as we will see in the discussion of vaccines in Unit 5, the feeling of sickness after vaccination is not caused by host cell damage or infection, but rather the perception of infection by cells of the immune system. The main point here is to flush out the difference between direct and indirect damage to the host. Direct damage is caused when the pathogen replicates, or when the pathogens release toxins that cause host cell death. Direct damage is most clearly demonstrated by intracellular bacteria and by viruses. In addition, many pathogens make factors that subvert the immune response to prevent clearance. Although this is not the focus here, it is important to mention. 1Lesson Unit4.1 7

8 3. Lecture & Socratic Discussion Indirect damage is caused by the immune response to the toxins and to other molecules the pathogens release. Generally, immune cells will intentionally lyse host cells in order to gain access to the pathogen. In fact, in some cases bacteria use this response to damage host cells and gain access to other areas of the host. For instance, Streptococcus can invade the bloodstream by using immune responses to damage epithelial cells in the lungs. 1Lesson We will discuss details of how the immune response damages host cells in Unit 5. Definitions of indirect and direct damage: Direct damage: Mainly caused when bacteria and viruses replicate intracellularly and cause host cell lysis. Also caused when bacteria and parasites make enzymes and factors that damage the host. The pathogen often uses these enzymes to enter new spaces in the host. Indirect damage: Mainly caused when bacteria replicate extracellularly. Also caused when activation of the immune response leads to damage of infected and bystander host cells. (The details of this will be discussed in unit 5). Bacteria often use the immune response to damage the host so they can migrate into new places in the host (exo and endo toxins are good examples of this). As mentioned in the last slide, pathogen localization and replication impacts the mechanism of host cell death. Ask the students: Define extracellular and intracellular. Extracellular means outside the cell whereas intracellular means inside the cell. You should emphasize correct usage of the prefixes because they are commonly used in science. The video clip shows intracellular bacteria moving inside a host cell they have infected. Unit4.1 8

9 3. Lecture & Socratic Discussion Where bacteria are located in the host has extensive implications for how disease is experienced. The implications of the location of bacterial growth are extensive and will be explored here. The implications for the immune response will be discussed in Unit 5. than any other human pathogen. Important points: Bacteria that replicate extracellularly are more adaptable than those that replicate inside cells. Not only are they poised to migrate to a new location if nutrients become depleted, but they usually do not require host cells so they can survive outside of a host until they infect a new host. S. Aureus is an example we have studied before. For example, many extracellular bacteria can survive on inanimate objects and surfaces, such as bedding, clothing, doorknobs, and in other environmental places like water. Cholera is an example we have studied before. Hence, extracellular pathogens may not require host-to-host contact to be transmitted. Again cholera is a good example. Ask the students: The bacteria illustrated on the slide are Staphylococcus aureus, the most common of the pus-producing or pyogenic bacteria. The students may remember this bacteria from the nasal swab activity in Unit 2. They are among the most adaptable of all pathogens. They are one of the hardiest of the non spore-forming bacteria and can survive for long periods on dry surfaces and, coexist with humans in almost any environment. They are difficult to eradicate, and are responsible for many community- and hospital-associated infections. Staph. Aureus causes more frequent and varied types of diseases Are extracellular bacteria visible to immune cells? If so, what would the result be? Yes and so they can cause indirect damage to the host. Can extracellular bacteria cause direct damage? They can if they produce a factor like a toxin. If the toxins can cause lysis of host cells, they can gain access to new areas of the host. Bacterial toxins like this will be the main focus of the next lesson. 1Lesson Unit4.1 9

10 3. Lecture & Socratic Discussion (just like a virus). This is an excellent illustration of direct damage. Are intracellular bacteria are visible to immune cells, and if so what the result would be? Immune cells can detect the intracellular bacteria (T cells do this). They can then cause indirect damage if they lyse the host cell. Most bacteria that replicate intracellularly do so because they depend on specific nutrients that the host cell supplies. A good example are the Chlamydiae. Chlamydiae are smaller than other bacteria ( microns compared with the 1 micron E. coli). Surprisingly enough they are auxotophic for (unable to make) three of four nucleoside triphosphatases (ATP, GTP and UTP). In fact, their requirement for host ATP has led them to be called energy parasites. They are also unable to synthesize several amino acids including cysteine and tryptophan. Chlamydiae are gram negative. Because intracellular bacteria use host cell nutrients, they are less susceptible to nutrient depletion than extracellular bacteria. They are also able to evade the immune system very effectively by camouflaging themselves inside the host cell. Since intracellular bacteria require a host cell to survive, Chlamydiae are usually transmitted from host to host. Walk the students through the lifecycle of chlamydia and emphasize indirect and direct damage. More about chlamydia: Chlamydia infection produces very subtle symptoms, mostly a little inflammation which progresses from the cervix to the endometrium, to the fallopian tubes and finally to the peritoneum. By the time symptoms appear in the peritoneum it is likely that the fallopian tubes are severely affected, leading to irreversible infertility. These women are at risk for life - threatening ectopic pregnancies. In addition, infants born vaginally to infected women acquire chlamydia in their eyes, ears nose and mouth and develop mild conjunctivitis together with a chronic cough. Untreated approximately 2/3 of infected children suffer long-term respiratory abnormalities including asthma. In men, inflammation of the urethra progresses to the prostate gland. Ask the students: How do intracellular bacteria cause direct damage? The bacteria spread when they are in need of more nutrients. They 1Lesson replicate and cause hose cell lysis to release the newly grown bacteria Unit4.1 10

11 3. Lecture & Socratic Discussion Ask the students: What stages may lead to direct or indirect damage? Direct - when the bacteria lyse the host cell to spread. Indirect- when immune cells, like T cells, kill infected host cell. The life cycle of chlamydia 1. Chlamydia grows in the epithelial cells of the mucous membranes of the eyes and genitals. 2. The infectious form is called an Elementary Body (EB). Infection begins when the EB attaches to the apical (outside) surface of the epithelial cells. Then it is endocytosed. 3. Once inside the cell the EBs quickly modify the endosomes they are in, thereby escaping from the pathway that is targeting it to the lysosome for destruction. Then, several of the modified endosomes fuse to form a microcolony called an inclusion. There may be multiple inclusions in each cell. 4. The EB then transforms into RB (reticular body) that are able to replicate. 5. They begin to replicate. The replication can be stopped by the immune responses or when the bacteria have consumed all of the host cell s nutrients. In the last unit students learned that the driving force for bacteria and parasites to invade a host is to gain access to nutrients. The faster bacteria replicate the faster they will need to migrate to a new source of nutrients. Hence, fast growing bacteria generally cause acute damage to a host because they have to gain access to new areas of the body in search of nutrients. Ask the students: What happens to bacteria when nutrient supply is exhausted? Cell division stops and the proportion of viable bacteria drops. How can the bacteria respond? 6. The bacteria then lyse the host cell in search of more nutrients. They can either navigate to a new environment or assume a This lysis may lead to further invasion of host cells or release to protective configuration, like a spore. 1Lesson infect other people. Unit4.1 11

12 3. Lecture & Socratic Discussion How might the rate at which a pathogen replicates impact illness? Pathogens migrate when they need to, so if bacteria grow quickly they will exhaust their resources and need to migrate. This migration then leads to host cell damage. Use the following two examples to illustrate the point that migration often leads to host cell damage: 1. If Streptococcus in the lungs need more nutrients they may attempt to bypass the thin lung epithelia to gain access to the blood stream. To do this the bacteria will need to damage the epithelial cells. 2. When Chlamydia exhausts the resources in a cell it lyses the cell, and migrates to another. When the bacteria attach to the intestinal lining they release toxins. These toxins cause direct damage by affecting the pumps in the intestinal lining that pump out the water. Because the bacteria grow quickly this damage is acute. The immune system responds vigorously because the bacteria are growing quickly. This in turn causes indirect damage which is also acute. Tuberculosis is a good example of how slow replication causes persistence of infection. 1Lesson Fast growing bacteria like cholera replicate quickly and so they cause acute illness. Acute illness can be caused by direct or indirect damage. Ask the students: How does cholera cause host cell damage? Cholera stays in the gut. It doesn t pass through the epithelial wall. However it pumps water out of the epithelial cells causing massive dehydration. The bacterium that causes tuberculosis, Mycobacterium tuberculosis is covered by a thick waxy coat, (i.e. it is Acid fast). This coat makes it difficult for nutrients to diffuse in, and so its replication is much slower than normal pathogens: hours compared with less than one hour for most other pathogens. Because Mycobacterium tuberculosis replicates slowly it does not need to migrate to new host cells frequently. In fact, it generally stays in a small number of cells that become surrounded by immune cells that wall it in forming a granuloma. Unit4.1 12

13 3. Lecture & Socratic Discussion A granuloma is mass of immune cells that form when the immune system attempts to wall off a pathogen to prevent its spread. This point is further discussed in the next slide. More about tuberculosis: Almost all tuberculosis infections occur from inhaling the aerosols made when an infectious person coughs, sneezes or talks. Ask the students: Do you think tuberculosis bacteria in granulomas can be seen by the immune system? Pathogenesis of tuberculosis: 1. Mycobacterium tuberculosis is exceptional because it can replicate both inside and outside of cells. When the bacteria enter the lungs and are ingested by macrophages they carry on dividing inside the macrophages, killing them, rather than vice versa. 2. At this point the immune system moves in to wall off the areas of infection from the rest of the lung into granulomas. ing seen by the immune system. This is why most people infected with TB often have no symptoms. 4. However, if the immune system becomes compromised, for example during aging, following stress or after another infection like HIV, the TB infection can become reactivated. If the bacteria become reactivated the granulomas may burst, releasing bacteria, which then begin to divide, infecting other cells and potentially other people. 4. Wrap Up Emphasize that we get sick because of cellular damage! Ask the students: Why do bacteria damage their hosts? 3. Mycobacterium tuberculosis can survive for long periods without To get access to nutrients. 1Lesson replicating in granulomas, thus not damaging the host and not be- Unit4.1 13

14 4. Wrap Up 5. Homework Briefly review the types of damage. Ask the students: Which type of bacteria normally cause direct damage? This is mainly caused by replication of intracellular bacteria. How can extracellular bacteria can cause direct damage? Bacteria and parasites can make toxins and factors that damage the host. Which type of bacteria normally cause indirect damage? This is mainly caused by extracellular bacteria. The readings in preparation for the jigsaw activity are in the material folders of lessons 4.1 and 4.2. How can bacteria cause indirect damage? By causing the immune system to damage the host. What is the purpose of direct and indirect damage? They often serve to allow the microbe to enter new spaces in the host. In this lesson we mentioned that bacteria have tools like toxins that help them damage their hosts directly or indirectly. These toxins will be the focus of the next lesson. The reading assignment about toxins is in preparation for a jigsaw activity in the next lesson. If today s class ends early the students can begin their homework. The reading is in the materials folder for this lesson and unit Lesson Unit4.1 14

15 Outline OVERVIEW Rationale: In the last lesson the students learned that pathogens cause illness by damaging the host via cell lysis. Although many symptoms, like fever and swelling, result from immune responses like cytokines, pathology results from host cell damage. We also discussed the difference between direct and indirect damage and focused on the impacts that bacterial replication has on host cell damage. This lesson continues to explore how bacteria cause damage to host cells. The last lesson focused on cell damage that results from bacterial replication, this lesson focuses on how bacterial toxins damage the host. Although some toxins damage the host directly, others stimulate immune responses that lead to indirect damage. For example, LPS that is a component of the bacterial cell wall causes damage by activating innate immune cells. It is also important to emphasis that the toxins perform a function for the bacterial life cycle. Do Now: This do now offers the students a chance to put the functions of toxins into a context relating to host cell damage. Jigsaw Activity: This activity will give students the opportunity to learn about a number of toxins and to discover the functions of the toxins in an inquiry based setting. Wrap Up: In the next lesson we will see how bacteria acquire tools like toxins. The wrap up offers a chance for students to reflect on this. The Lesson Plan Toxins: Botox, tetanus, hamburger disease and MRSA. 1. Do Now (10 min): Have the students brainstorm what they learned yesterday about how bacteria damage the host with an emphasis on host cell lysis, direct damage (replication and toxins), and indirect damage (when self cells become a casualty). 2. Activity (20-25 min): Jigsaw about bacterial toxins. 3. Wrap Up (5 min): Pose a question for reflection: How can pathogenic bacteria bypass the host defenses when most bacteria can t? This will lead us into the next lesson. 2Lesson 2Lesson Unit1.2 Unit4.2 15

16 1. DONOW All of these images have toxins in common! Ask the students to look at the images in the next few slides while trying to answer the question: What is the common link between the following images? Hamburger: Food poisoning may result from eating uncooked meat that is contaminated with E. coli 0157:H7. Unlike the commensal E.coli in our intestines pathogenic E.coli secrete Shiga toxin. Man with tetanus: The person in the image looks like they are being electrocuted because they have been infected with clostridium tetani that produces tetanus toxin and are suffering prolonged skeletal muscle spasms. Angelina Jolie: Botox is a drug made from the botulinum toxin produced by clostridium botulinium. Botox blocks the muscle contraction that causes wrinkles, but can also inhibit breathing. Leg rash: The inflamed swollen rash was caused by methicillin-resistant Staph. Aureus (MRSA). MRSA produces a toxin that activates immune cells, thereby causing indirect damage to the host. 2Lesson Unit4.2 16

17 2. Activity new tissues. Killing competing bacteria. Jigsaw Activity The readings for the Jigsaw activity are in the materials folder of this lesson. 2Lesson To this point we have described toxins as molecules that bacteria release or express in order to manipulate the host. We have also discussed the idea that bacteria use these toxins to migrate within a host to gain access to nutrients. Before starting the jig-saw activity, ask the students: What is a toxin? A toxin is a poisonous substance, usually a protein or lipid, that is produced by living cells or organisms and is capable of causing disease when introduced into the body tissues. Also, a toxin is not a pathogen, in part because a toxin does not replicate. How might bacteria use a toxin? Bacteria use toxins to gain access to nutrients. How might they gain access to nutrients? Directly damaging host cells to invade new tissues. Indirectly damaging host cells by eliciting immune responses to invade The materials for this activity are in the materials folder for this lesson. Procedure: 1. Assign each student to a group so that each group has a representative who will be studying one of the 5 assigned bacteria. 2. Give each student an article and a blank worksheet (ID- Handout) to be filled out during the activity. 3. Give students time to read their articles. Each article should have a number group, 1-6, on the top corner to be used later. 4. Have students read the article and complete the worksheet. 5. Have students discuss their article with in their expert groups. Unit4.2 17

18 2. Activity 6. Once the students have become experts, have the students break out into their number group and TEACH! Each of the number groups should have an example of the five different bacteria. Jigsaw Activity 7. As the students complete their teaching, have the student devise two possible questions that could be used on an assessment. Submit the 2 questions for the teacher. (You could use the assessment questions as a DO NOW for the following day.) 3. Wrap Up The readings for the Jigsaw activity are in the materials folder of this lesson. Ask the students: How come pathogenic bacteria are able to make toxins? Bacteria are under immense pressure to acquire nutrients, so they have evolved / adapted these tools. We will discuss the process of bacterial 2Lesson adaptation in the next lesson. Unit4.2 18

19 Outline OVERVIEW Rationale: The lessons thus far have emphasized that pathogenic bacteria are microbes that find a way to enter the body and cause damage. This is in contrast to most microbes, which are effectively dealt with by the immune system. So that leaves the question: How do bacteria become pathogenic? This lesson will focus on this question from the perspective of adaptations that give bacteria the ability to bypass different barriers of the immune system. Do Now: The do now leads the students to the conclusion that pathogens need special tools to bypass host immune barriers. Bacterial Adaptation Auction: In this activity students bid on an adaptation in an attempt to design a successful pathogen. This activity illustrates that different adaptations offer select advantages and perhaps disadvantages. Many of the adaptations in the auction were introduced in Unit 1. In this activity, the focus should be on further understanding the functions of the adaptations from the perspective of gaining accesses to nutrients and causing host cell damage. In addition, the use of the auction is meant to emphasize that having adaptations cost the bacteria energy which slows growth. Nothing in life is free! Wrap Up: The worksheet asks the students to think deeply about the functions, both advantageous and disadvantageous, of the toxins. If you are short on time the worksheet can be finished as homework. The Lesson Plan How do bacteria adapt to become pathogens? The adaptation auction 1. Do Now (10 min): We have defined a pathogen as a microbe that can enter the host and cause damage. Lead the students to the conclusion that bacteria need adaptations to evade host defenses (entry and camouflage). 2. Activity (20-30 min): Bacterial adaptation auction: Further explore the uses of adaptations to gain accesses to nutrients and to cause host cell damage; emphasize that bacteria cannot have infant adaptations; having adaptations cost the bacteria energy which slows growth. 3. Wrap Up (10 min): Complete the worksheet to hand in at the end of class. 2Lesson3Lesson Unit1.2 Unit4.3 19

20 1. DONOW Help the students list the different bacterial structures that they learned in Unit 1. Ask them to think about each of the structures and how they might provide the bacteria with an adaptive advantage. Ask the students: What do microbes need to become pathogenic? Pathogens have evolved tools that will allow them to bypass host defenses. These tools are called adaptations. Many of the adaptations used in the auction were introduced in Unit 1. In this activity, the focus should be on further understanding the functions of the adaptations from the perspective of causing host cell damage in order to gain access to nutrients. In addition, the auction is meant to emphasize that having adaptations costs the bacteria energy, which in turn slows growth. What adaptations might a microbe need to become a pathogen? Pathogens need to be able to invade the host and stay camouflaged to avoid the immune system if they are to persist in the host. 3Lesson Unit4.3 20

21 2. Activity Instructions for the Bacteria Adaptation Auction: Assign students to teams of 2 to 4 (6 to 8 teams total). The worksheet for the Bacteria Profile is in the materials folder of this lesson. 3Lesson Bacterial Adaptation Auction Students will be divided into teams and each be given a habitat. Their goal will be to design a bacterium with the best chances of survival and reproduction. During the auction teams will bid on adaptations for their bacterium. In-class assignment: Bacteria Profile As the students are participating in the auction have them answer the following questions on the worksheet and collect their work at the end of class. 1. Name your bacteria (Genus and species). 2. Describe your bacteria s environment. 3. Draw your bacteria showing the adaptations you bid on. 4. Explain why your adaptations will help your bacteria survive and reproduce in its habitat. The worksheet is in the materials folder for this lesson. Bacterial Habitats: Before beginning the auction, assign each team a specific bacterial habitat. This habitat will give students a context for deciding what adaptations would be most useful. Suggested habitats: 1. Intestines (colon) 2. Blood 3. Lungs 4. Nasal Passage 5. Eyes 6. Skin Bacteria Auction: Give the teams a list of the adaptations available (this is the second page of the student worksheet). The students will discuss the adaptations they feel will be most important for their bacteria s success, thinking specifically about their assigned habitat (5-10min). Each team will have $1000 to spend on adaptations. The teams should strategize how much money they are willing to spend on their favorite adaptations. Since some adaptations are particularly useful, some of them will be offered more than once during the auction. The auction is given in the form of a ppt, which comprises the remaining slides in this lesson. Unit4.3 21

22 2. Activity Auction Schedule: Gram negative bacteria LPS (salmonella), Flagella (megingitis) Gram positive bacteria murein layer, spore formation Acid-fast cell walls contain large amounts of waxes laced with murein, sugars, and lipids so they avoid white blood cells and resist chemicals well (M. tuberculosis) Low replication rates survive for long periods in granulomas (M. tuberculosis) High replication rates infection can spread quickly from host to host (Cholera) Extracellular replication adapt quickly by migrating to new areas when nutrients become depleted (S. aureus). Intracellular replication take nutrients from host (Chlamydiae) Conjugation gain antibiotic resistance using new genetic information from other bacteria Cell lysis destroy host cell (Plasmodium) Produce exotoxins secrete proteins into surroundings to aid survival and spread (Cholera, Shiga toxin) Produce exoenzymes break down matrix surrounding cells to spread more rapidly (Streptococci pyrogenes) Produce endotoxins part of the cell wall 3Lesson Unit4.3 22

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28 3. Wrap Up Also emphasize that in nature adaptations are acquired randomly and then selected by improved growth, as opposed to being chosen. Challenge the studnets to consider: The worksheet is in the materials folder of this lesson. Why couldn t you buy all the adaptations? There are energy costs to making everything, so excess adaptations may slow growth and make the bacteria less fit. Have each student complete their worksheet. If you are short on time, the worksheet can be finished as homework. 3Lesson Unit4.3 28

29 Outline OVERVIEW Rationale: This lesson extends the principles learned in Unit 4.1 by addressing how viruses cause host damage. It focuses on how viruses replicate, and then exit from host cells. The lesson also introduces the difference between DNA and RNA viruses and explains that viruses need host proteins to replicate. Furthermore, the virus may damage the host cell during replication, either directly or indirectly, as we saw with intracellular bacteria. Do Now: In Unit 1.4 the viral structures and some aspects of viral life cycle were described. In this do now we will extrapolate on that information to explore how viruses cause host cell damage. Lecture and Socratic Discussion: This activity introduces the viral life cycle and focuses on viral genome replication. One goal of the discussion is to have students use their knowledge of bacteria-mediated damage to predict how a virus might causes damage. Wrap Up: This lesson contains a large amount of information about viral replication and host cell damage. This wrap up re-caps the important concepts. It may also be useful for students to re-write their notes from class and hand them in as a homework. The Lesson Plan How viruses make us sick: viral replication 1. Do Now (10 min): Ask students to recall the two ways a pathogen causes damage (direct vs. indirect). Brainstorm: How do you think a virus causes damage to the host? 2. Lecture/Discussion (25-30 min): Powerpoint presentation of viral replication and host damage. 3. Wrap Up (5 min): Review the main learning objectives. 2Lesson4Lesson Unit1.2 Unit4.4 29

30 1. DONOW Before proceeding we will review the two ways that host cells are damaged. Indirect damage results from immune responses to the infection. This may happen when an infected cell is killed intentionally or when bystander cells become casualties. Ask the students: What are the two ways a pathogen causes damage to host cells? Direct and indirect. Ask the students: What is the common feature of both types of damage? The students should recall that both types of damage result from lysis of host cells. Ask the students: What does direct and indirect damage entail? Direct damage occurs when an intracellular pathogen causes host 4Lesson cells to lyse when it replicates or when it releases toxins. Unit4.4 30

31 1. DONOW 2. Lecture and Discussion Ask the students: What features of a virus will affect how it causes damage to the host? The students should be able to use their knowledge of the viral life cycle to answer this question. Viruses replicate in host cells, like intracellular bacteria. Therefore a virus can directly damage host cells by depleting their nutrients and by causing the cell to lyse when it exits the host cell. Viruses can indirectly damage host cells when T cells kill the infected cell. This may happen when an infected cell is killed intentionally or when bystander cells become casualties. In Unit 1.4 the students learned about viral structure and were introduced to viral life cycles. This discussion focuses on viral replication and at the end of the discussion we emphasize that viruses cause damage when they exit the host cell. 4Lesson Unit4.4 31

32 2. Lecture and Discussion The main principles of this lesson are: How Viruses Enter the Cell 1. Viruses are designed to make more virus. 2. Viruses use the cell s machinery to to replicate its genome (RNA or DNA) and to make proteins. 3. The virus then assembles with the help of the host cell, and is ready to spread to a new host cell. 4. Viruses exit by budding out of the cell, stealing part of the cell membrane, or by lysing the cell. How Viruses Make Us Sick Have the students recall what they know about viral entry from Unit 1.4. All viruses need to make protein so they can assemble the delivery device (the capsid and, if present, the envelope) that makes a new viral particle that can deliver the genome to a new cell. For this assembly to take place viruses use the normal processes by which host cells synthesize DNA, RNA, and protein. 1. Viruses must attach to a host cell before it can penetrate the membrane. 2. Attachment: The virus attaches itself to its host cell through interactions between a protein on its surface and a complementary receptor on the host cell membrane. 3. Remind the students that virus-host interactions involve specific receptors that determine the type of cell the virus can infect. 4. We should note that receptors on the host cell that viruses attach to are not there simply for benefit of the virus, rather they play important physiological functions for the cell. We use Influenza and HIV as examples. 5. Naked and enveloped viruses enter the host cell in slightly different ways: a. Naked - receptor mediated endocytosis. b. Enveloped-receptor mediated fusion with the membrane. 4Lesson Unit4.4 32

33 2. Lecture and Discussion Examples of attachment: Viral Replication The influenza receptor 1. The receptor for the Influenza virus is a sugar (sialic acid) that is found on many cell types. 2. Influenza virus enters the body in aerosols, so it will infect the first cells it comes into contact with that carry the sugar. These are epithelial cells lining the respiratory tract. 3. Different animal species have different versions of this sugar on their cells, and this determines which species various serotypes of virus can infect (e.g. swine flu, avian flu, etc). 4. The protein on the influenza virus that interacts with the sialic acid receptor is Hemagglutinin. Hemagglutinin is the H in H1N1. 5. Different serotypes of virus have different Hemagglutinins that recognize different sugars so, for example, the H1 in H1N1 recognizes a different sugar than the H5 of the H5N1 (avian influenza) recognizes. 6. Interestingly, the cells in our upper and lower respiratory tract express different types of these sugars, so H1N1 can infect the upper respiratory tract, whereas H5N1 can infect the lower respira tory tract. This explains why H1N1 causes less severe illness in humans than H5N1. The next few slides focus on the processes involved in viral replication after the viral genome is in the host cell cytoplasm. During the process of replication the viral genome duplicates itself many times, viral proteins are made and the virus is assembled. This process can compromise the infected cell because its resources are diverted to making virus. How replication occurs depends on the type of genome that a virus has. HIV receptors 4Lesson 1. In contrast with influenza, the HIV receptor, CD4 is found on only two specific types of immune cells. 2. When HIV interacts with CD4 and infects T cells and they are ir reversibly damaged. 3. This is reflected in a reduction in immune system function leading to AIDS (Acquired Immune Deficiency Syndrome). Unit4.4 33

34 2. Lecture and Discussion To help students better understand how the different types of virus replicate in cells we will first revisit molecular dogma. Molecular dogma explains the process of protein synthesis from DNA. Students should be completely clear about how this happens before proceeding. 1. DNA can be copied. 2. This DNA is used to make complimentary sequences of RNA. 3. The sequence of the RNA is used to make corresponding amino acid chains that fold into functional proteins. 4. The proteins perform the functional activities of the cell. As shown in the figure in the slide, it is important to note that DNA directly codes for RNA in a base by base manner, while RNA uses codons (three nucleic acids translates into one amino acid) to code for amino acids. Each amino acid may have more than one slightly different codon. This means that mutations in DNA and RNA don t always translate into changes in amino acid sequence. Ask the students: Where in the cell do these processes take place? The processes are called: 1. DNA replication- DNA can be copied. 2. Transcription- The sequence of the DNA is used to make complimentary sequences of RNA. 3. Translation- The sequence of the RNA is used to make corresponding amino acid chains that fold into functional proteins. Use the slide to describe where replication, transcription, and translation take place. Point out that a viral genome must be in the correct location in the cell to use its machinery. 4Lesson Unit4.4 34

35 2. Lecture and Discussion Ask the students: What steps will the virus have to take if its genome is DNA? In that case the virus can use the host cell machinery that is normally making host cell proteins from RNA. Could the virus use the host machinery if its genome is RNA? Host cells copy DNA but they can t copy RNA (RNA is made from DNA in a base by base manner) So the viruses must have an alternative way to copy an RNA genome if they want to replicate. Since DNA viruses use DNA, they need to be in the nucleus to access the transcription apparatus of the cell. In fact, all viruses that use DNA need to enter the host nucleus. Just like host genes, the viral genome follows molecular dogma. Hence, host proteins are used: 1. DNA polymerase performs DNA replication. 2. RNA polymerase performs transcription. 3. Ribosomes perform translation. But if a virus needs to do something that a host cell cannot, the virus must enter the host cell with the necessary proteins to be able to do it for itself this is dealt with in the next few slides. Ask the students: Host cells cannot copy RNA, they can only make RNA from DNA, so how does an RNA virus replicate its genome? 4Lesson Unit4.4 35

36 2. Lecture and Discussion The virus brings its own enzyme that can make RNA from RNA (RNAdependant RNA polymerase). This protein is unique to each virus so and so it may be a good target for drugs to interfere with its function! Ask the students: Would reverse transcriptase make a good drug target, and if so, why? A successful drug will damage the pathogen but not the host cell. Reverse transcriptase is a good drug target because it isn t a normal host cell process. HIV is an example of a retrovirus. A number of successful HIV drugs target the reverse transcriptase. When DNA or RNA is replicated, random errors arise at a rate of about 1 in 100,000 base pairs. However multiple codons with different nucleotide sequences code for each amino acid so these errors may have no effect on the eventual protein that is produced (this is called a silent mutation). Yet, mutations that change the amino acid sequence and structure of the protein might affect pathogenesis. Eukaryotic cells have devised strategies to correct for errors during DNA transcription. They have a DNA proofreading enzyme that reduces the error rate 1000 fold to 1 in 100 million. DNA viruses, which use host machinery can also take advantage of this proofreading enzyme, and as a result have a relatively low rate of mutation. In contrast, RNA viruses lack their own proofreading enzyme or repair mechanism. Therefore mutations in RNA viruses are quite common. To counter the potential disadvantages of mutation, RNA genomes generally have a smaller maximum size than DNA viruses. Beyond this limit, the high frequency of replication errors will make the virus useless, uncompetitive, or more virulent. Ask the students: Can you think of mutations that would be beneficial to the virus? The mutations are randomly and most damage the virus, but some could be beneficial. For example, a mutation it could make a hemaglutinin molecule more likely to bind to the host cell. 4Lesson This process of random mutation is called antigenic drift. Unit4.4 36

37 2. Lecture and Discussion Viral mutation and adaptation will be the focus of the next lesson. 3. Wrap Up Once replication has occurred the virus must leave the host cell to carry on its cycles of infection. Like viral entry, viruses have different exit strategies if they are enveloped or naked and both strategies eventually lead to cell death. Reiterate the points of the class: Have the students recall the process of viral exit for enveloped and naked viruses: Enveloped viruses are able insert their envelope proteins into the plasma membrane of the host cell. Then the genome and capsid assembles beneath the area where the envelope proteins have been inserted. They push out or bud through the membrane, assembling the capsid and the envelope as they do so. This is true of both HIV and influenza. Naked viruses use the same principle as all non-enveloped viruses. Quite simply the huge numbers of virus particles that accumulate in the cytoplasm break open the cell by force (lysis). So naked viruses always cause host cell lysis. 1. Viral entry utilizes receptors on host cells. 2. Enveloped viruses enter cells by fusing with the plasma membrane or through endocytosis. 3. Naked viruses enter host cells by injecting their contents into cells or through endocytosis. 4. DNA viruses replicate with the host s transcription and trans lation machinery. 5. RNA viruses carry special enzymes to copy their genome. 6. Enveloped viruses exit the host cell by budding. 7. Naked viruses exit the host cell by lysis. Emphasize that viruses cause direct damage when they exit cells and indirect damage when T cells kill infected self-cells. 4Lesson The cell debris will attract an immune response. Unit4.4 37

38 Outline OVERVIEW Rationale: This lesson will further explore how viruses cause disease by focusing on how they adapt in order to enter and infect the host. The lesson also describes the processes of antigenic drift and shift and then asks students to apply this knowledge to complete a case study about how flu vaccines are designed. Do Now: In the do now students will use their knowledge of bacterial adaptations to predict viral adaptation; viruses adapt to avoid immune pressure and infect more hosts. Lecture and Socratic Discussion: This discussion will give students an opportunity to learn about viral adaptations by extrapolating from what they have learned about bacterial adaptations. Flu Vaccine Worksheet: This activity illustrates how antigenic drift and shift impact the human experience with influenza. Wrap Up and Homework: To solidify what was learned today the students will be able to use the wrap up time to ask questions about the worksheet. They may finish the worksheet as homework if needed. The Lesson Plan How do viruses adapt? antigenic shift and drift and the flu pandemic 1. Do Now (10 min): Have the students brainstorm the types of adaptations a virus may need to optimize infection. Help the students come to the conclusion that viruses, like bacterial pathogens, need adaptations to evade the host s defenses (entry and camouflage). 2. Lecture/Discussion (15-20 min): How viruses mutate: antigenic drift and antigenic shift. 3. Activity (15 min): Demonstration: Modeling antigenic shift in the influenza virus. Flu vaccine worksheet. 4. Wrap Up and Homework: Flu vaccine worksheet. 2Lesson5Lesson Unit1.2 Unit4.5 38

39 1. DONOW 2. Discussion Ask the students: The 1918 flu appeared suddenly and killed millions of people. Where does a virus able to cause such a catastrophic pandemic come from? Viruses, like bacterial pathogens, mutate randomly every time they replicate. Mutations can have one of 3 effects: 1. The mutation can have no effect. 2. The mutation can produce a virus that is defective in some way. 3. The mutation can help the virus cause worse disease or spread better. The next few slides prepare the students for a worksheet covering antigenic drift and shift in the context of the flu vaccine. Antigenic Drift and Antigenic Shift Viruses mutate in two different ways called antigenic drift and antigenic shift. Antigenic drift is the name given to the random mutations that accumulate during replication. These mutations produce alterations to individual bases in the virus genome. DNA viruses use the host proofreading enzymes to correct these mutations. In contrast RNA viruses can t proofread when copying their genomes. Ask the students: 5Lesson Why not? RNA viruses replicate RNA and reverse transcriptase lack host cell proofreading capacities. Unit4.5 39

40 2. Lecture and Socratic Discussion In RNA viruses random antigenic drift means that the viruses of the same species often exist as swarms - with slightly different genome sequences called quasispecies. Within quasispecies an individual virus with a competitive advantage will take over the population by natural selection. Antigenic shift allows one virus to exchange actual genes with another virus. These exchanges lead to dramatic changes in the virus structure. Remind students that H1N1 was known as swine flu. Ask the students: Can you imagine a way that antigenic drift could cause dangers associated with flu? If a strain of flu that infected swine acquired a gene that would allow it to infect humans then humans would be exposed to a strain of flu they d never experienced before. Define both: Drift: Random mutations caused by errors in proofreading. Shift: Exchange of genetic information between viruses. Antigenic drift is a gradual process, which often has no effect on virus function. Antigenic shift causes large changes that may increase or decrease virulence. Non-Segmented Genomes Another way? If the virus acquires a gene that allows it to infect another part of the respiratory system then it could cause worse disease. For example avian flu infects epithelial cells much lower down in the lungs. And so causes much worse symptoms when the immune system responds it causes a vast influx of fluid into the lungs which essentially causes people to drown. This cartoon shows that a virus with a non-segmented, or continuous genome, cannot exchange genetic information with another virus. Explain the cartoon to the students: 1. The blue pentagon depicts the viral capsid. 2. The stars on the surface of the capsid represent viral entry receptors. 3. The black and red lines within each capsid represent the viral 5Lesson Unit4.5 40

41 2. Lecture and Socratic Discussion cell the genomes of the daughter viruses look similar to the genomes of the parent viruses. In this case they non-segmented i.e. single strands of either RNA or DNA. These viruses can only mutate by antigenic drift. 4. The tan shape represents a host cell. It can be infected by more than one virus. 5. When two viruses with non-segmented genomes infect one host Segmented Genomes This cartoon shows that a virus with a segmented genome can exchange genetic information with another virus. 4. The tan shape represents a host cell. It can be infected by more than one virus. 5. When two viruses with segmented genomes infect one host cell the genomes of the daughter viruses may look differ- ent to the genomes of their parent viruses because they can exchange parts of their genome with each other. Antigenic Shift This figure ties in how the genes exchange with the consequences of the exchange on the surface. The concepts in this slide will also be covered in the demonstration. Explain the cartoon to the students: 1. The blue pentagon depicts the viral capsid. 2. The stars on the surface of the capsid represent viral entry receptors. 3. The black and red lines within each capsid represent the viral genomes. In this case they segmented i.e. the genome is in discrete pieces or segments. These viruses can mutate by antigenic drift, but they can also mutate by antigenic shift. 5Lesson Unit4.5 41

42 3. Activity Demonstration: 4. Wrap Up Worksheet: The protocol for this demonstration can be found in the materials folder for this lesson. This demonstration can also be give to the students to use as a hands-on learning aid. The worksheet can be found in the materials folder of this lesson This worksheet should be finished as homework. The worksheet and the protocol for the demonstration are in the materials folder of this lesson. 5Lesson Unit4.5 42

43 Outline OVERVIEW Rationale: In the last two lessons we discussed the relationship betwee the viral life cycle and host cell damage. We also saw that viruses mutate quickly via antigenic drift and shift. These mutations may enable the viruses to better enter/exit a host and/or to stay hidden from the host s defenses. This lesson offers students the chance to apply what they have learned thus far to design an anti-viral drug to treat HIV. Do Now: The do now orients the students for the activity by discussing the goals of the class. Activity: HIV video: The video demonstrates a model of how HIV replicates and re-infects a host. The students can use this model to develop their own anti-viral drug targets. Design an anti-viral drug: The students will develop their drugs in small groups and prepare to present and defend the logic that they used when designing the drug. Homework: The homework allows the students another opportunity to critique their drug design. The Lesson Plan Designing an antiviral drug the challenge of HIV. 1. Do Now (10 min): Discuss the goals of the class: we have learned about how viruses make use sick, so what can we do to treat a viral infection? What if that infection is HIV? 2. Activity (30-35 min): Design an anti-viral drug: Watch a short video to introduce a model of HIV replication and spread. Then have the students break into groups to design an antiviral drug and prepare to present their ideas to the class in a 2-3-minute presentation. 3. Homework: Have the students research anti-viral drugs used to treat HIV and write an evaluation of their initial drug design. 2Lesson6Lesson Unit1.2 Unit4.6 43

44 1. DONOW 2. Activity 6Lesson Ask the students: We have learned about how viruses make use sick, so what strategies might we use to develop a drug that would treat a viral infection? You could develop a drug that disrupts viral entry, replication, or exit. In fact all anti-viral drugs target one of these stages. Because of this antiviral drugs are generally specific to a select kind of virus, unlike antibiotics. So you would need to know the exact virus that was infecting the patient. As we saw in unit 2, identifying the type of infection is not trivial. It is also important to emphasize that antibiotics will not treat a viral infection! What if that infection is HIV? The students may have heard about antiviral drugs for HIV. Do not discuss details about these drugs. The activity is focused on designing their own drug to combat HIV. Discuss the goals for the activity: Tell the students that we will be using our knowledge of viral life cycles to design anti-viral drugs for HIV. Overview of the Activity: 1. Have the students break into groups of 4 students. 2. Using only the attached diagram of the HIV lifecycle and the animations, have students determine at least three more stages in the lifecycle of HIV where a drug could be developed to prevent HIV from spreading in the body. 3. Have students draw and explain their group s response on a poster using a scientific approach. developing a hypoth esis and discussion of how they could test the hypothesis about how the drug would prevent the spread of HIV in an individual s body. 4. Emphasize that students should identify what evidence they would use to indicate that the drug was effective in blocking the HIV life cycle. 5. Have students present their findings to the class in the form of a 2-5 minute presentation. If the class is running over on time forgo the teach-back. Unit4.6 44

45 2. Activity The worksheet is in the materials folder of this lesson. The worksheet for this activity can be found in the materials folder of this lesson. HIV Video Introduce the topic by having students view the video HIV Immunity: Have students answer the following discussion questions as they watch: 1. How does HIV infect a cell? 2. Some individuals are resistant to HIV. Explain the mechanism of HIV resistance that is described in the video. 3. What is the benefit of studying the extreme situations in a viral infection? 4. What potential benefit does knowledge of resistance offer? Have students view the animation: HIV Life Cycle: html or Have students use the animation and worksheet to answer the following questions about the HIV life cycle: 1. Explain the role of the following molecules in the HIV life cycle: a. CD4 receptor b. CCR5 receptor c. Reverse transcriptase d. Protease e. RNA polymerase f. Integrase 2. Besides the nucleus, what cell organelles play a role in the HIV life cycle? 3. Why is there a high mutation rate in HIV? 4. Based on what you already know about genetics, what does it mean for the host cell, now that the viral DNA has become a part of the host cell genome? Why would this make HIV difficult to treat? 6Lesson Unit4.6 45

46 2. Activity Overview of the Activity: 3. Homework 1. Have the students break into groups of 4 students. 2. Using only the attached diagram of the HIV lifecycle and the animations, have students determine at least three more stages in the lifecycle of HIV where a drug could be developed to prevent HIV from spreading in the body. 3. Have students draw and explain their group s response on a poster using a scientific approach. developing a hypothesis and discussion of how they could test the hypothesis about how the drug would prevent the spread of HIV in an individual s body. 4. Emphasize that students should identify what evidence they would use to indicate that the drug was effective in blocking the HIV life cycle. 5. Have students present their findings to the class in the form of a 2-5 minute presentation. If the class is running over on time forgo the teach-back. Have students research basics of HIV antiviral treatments to write an evaluation of their initial drug proposals. The students should address how close each proposal was to an actual pathway that current drugs target. Students could include some of the challenges posed by antiviral treatments and HIV vaccine development. The following link may help you evaluate student ideas: Meds/Lifecycle_and_ARVs.jsp 6Lesson Unit4.6 46

47 Outline OVERVIEW Rationale: This lesson gives students an opportunity to exercise their cumulative knowledge about infectious diseases by having them draw parallels between select pathogens in the context of a Facebook quiz. Do Now: The do now is intended to orient the students for the Facebook activity. Facebook Quiz Activity: The activity will allow students to work with the information they learned about pathogens. This includes how pathogens spread, where they reside in the host, the requirements for survival of bacteria, viruses, and more. Wrap Up: Re-cap the dichotomous keys for bacteria and viral choices from the Facebook quiz. Students may notice exceptions that don t fit into the key. Encourage such criticism! The Lesson Plan Putting together the strategies pathogens use what kind are you? 1. Do Now (10 min): Describe the goal of the Facebook activity. 2. Activity (25-30 min): Facebook Quiz activity. After completion, have students break into groups to discuss how the quiz choice relates to the microbe (draw parallels). Have the students complete a questionnaire that draws parallels between the Facebook quiz and the pathogen they were assigned for the final project. 3. Wrap Up (5-10 min): Use the dichotomous key slides to re-cap the parallels between the Facebok quiz choices and the bacteria and viral choices. 2Lesson7Lesson Unit1.2 Unit4.7 47

48 1. DONOW Facebook Activity Prep: 2. Activity The class will take a Facebook style quiz where they answer two-choice questions. Depending on their answers to each question, they will be led through a dichotomous key that will end with them identifying the infectious disease they most resemble. The quiz powerpoint, student worksheet and teacher worksheet are in the materials folder of this lesson and are given as PDFs at the end of the lesson Powerpoint. The dichotomous key has human-themed questions that parallel an event that may happen in the life of a microorganism. For example, When it is cold out, how do you like to keep warm? Wear multiple layers or wear a thick sweater. This question parallels the distinction between a Gram Negative and Gram Positive bacteria. A Gram Negative bacteria has multiple layers in its cell membrane while a Gram Positive bacteria has one thick cell membrane. At the end of the quiz, each student will have identified the microorganism that matches their personality. In think, pair, share format each student will describe to a partner the choices they made and what pathogen this led them to be matched with. Then the teacher will choose three groups to share with the class what they discovered from their partner s results Have the students take the Facebook quiz. The Facebook quiz powerpoint, student worksheet and teacher worksheet are in the materials folder of this lesson and are also given as PDFs at the end of the lesson powerpoint. 7Lesson Unit4.7 48

49 3. Wrap Up Debrief (1) : Bacteria Post/project the flow chart of the choices the students had to make throughout the dichotomous key. At the end of each path are the individual pathogens the students could have been matched to by the survey. Debrief with the class about how the choices were made. Debrief (2) : Viruses Debrief with the class about how the key was set up. 7Lesson Unit4.7 49