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 1. How does the enzyme Streptokinase contribute to the virulence of strep pyogenes? Streptokinase lyses the blood clots that are part of the body's immune response. Blood clots contain the infection, and withut them, it is easier for an infection to spread. 2. What are some of the complications associated with Group A Strep? Group A, or Beta hemolytic, Strep causes complete lysis of the red blood cells, which causes localized and distant complications includingscarlet fever, rheumatic fever, and kidney disease. 1) How are streptococci classified? 2) What introduced vaccine led to an almost complete elimination of cases, with cases reported being about 100 per year and of those most were non-­‐vaccinated adults? (Hint: To start school you must have this vaccination) 1. Group A strep are alpha or beta hemolytic? beta hemolytic 2. What is the causative agent of strep throat? Streptococcus pyogenes 3. What is an S. Pyogenes capsule made out of? And what makes it anti-­‐phagocytic and non-­‐
immunogenic? It is made from hyaluronic acid, which is identical to host connective tissue. The host will not make a response to the hyaluronic acid of the capsule because it is not foreign to the host. This makes it anti-­‐phagocytic and non-­‐immunogenic. 1. What role do M proteins play in the spread of Strep pyogenes. 2. A patient comes to the emergency room complaining of sore throat and fatigue. The patient has a slight fever and a swollen neck. Upon examination you notice a whitish gray membrane on the back of the throat. A culture reveals variably shaped gram positive rods. What does the patient have? If left untreated what are the possible outcomes. What would you do to treat it? ) What are some of Koch's Postulates limits? 2) What are the two major streptolysins and what is there main function? 3) Which proteins play a role in the virulence of strep. pyogenes? A) F proteins B) G proteins C) M proteins D) a & c E) a, b, & c What receptor does the G protein block on antibodies? What are the two theories about R. fever? 1.) Where do "large" air particles or droplets most likely attach in a human? A. lower respiratory tract B. upper respiratory tract C. G.I. Tract D. None of the above 2.) Why can a person catch one disease over and over again like the common cold, but not others like typhoid fever? Why do HIV vaccinations fail even though antibodies have been created which can bind to the virus? So far all the antibodies created have bound to parts of the virus which can easily change making the immune response strain specific. How do interferon act as cellular vaccines? When the infected cell makes interferon and releases it, the interferon binds to other cells, causing them to express antiviral mechanisms, making them temporarily immune. Now that the virus can not immediately enter another cell it is exposed to our immune defenses, and if it is even slightly changed it becomes defective due to its inability to turnover proteins and heal itself. 1) How do Interferon alpha and Interferon beta work to help localize viral infections? 2) Given that there are a limited number of adenoviruses and rhinoviruses which cause the common cold-­‐-­‐ why is it that the population does not naturally come to an equillibrium; that is, why don't we as individuals become immune to these pathogens as we may other disease causing agents? 1. A cell infected by a virus will begin to produce Interferon alpha and beta, which are type I Interferons. Infected cells secrete this type of "cellular vaccine" and it spreads to neighboring cells. Why are they type I Interferons nicknamed "cellular vaccines?" 2. What are two recognition strategies for the immune system to recognize an intra-­‐
cellular infection? Please explain in depth. 1. When comparing the common cold to other infections, why do people commonly catch the cold over and over? 2. Why are rhinoviruses and adenoviruses so easily able to infect humans? 3. What 4 things does a cell do to attract other cells to the site of infections?