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NOTES: CH 35 The Immune System and Disease. CH 35: Key Terms / Concepts Key Terms –Infectious disease –Pathogen –Antigen –Antibody –Immunity –Vaccination.

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Presentation on theme: "NOTES: CH 35 The Immune System and Disease. CH 35: Key Terms / Concepts Key Terms –Infectious disease –Pathogen –Antigen –Antibody –Immunity –Vaccination."— Presentation transcript:

1 NOTES: CH 35 The Immune System and Disease

2 CH 35: Key Terms / Concepts Key Terms –Infectious disease –Pathogen –Antigen –Antibody –Immunity –Vaccination Concepts –What causes infectious diseases and how do they spread? –How do our bodies respond to these pathogens? –How do we prevent infectious diseases to spread?

3 35.1 – Infectious Disease PATHOGEN: a disease-causing agent; disrupt normal body functions -pathogens include: virusesfungi bacteriaprotozoans

4 Examples of viruses: Small pox Polio Herpes Common Cold

5 How are Diseases Spread? Coughing, sneezing, physical contact Exchange of body fluids Contaminated food and water Animal contact (zoonosis) -VECTOR = an organism that transports the pathogen, but does not get sick.

6 35.2 – Defenses Against Infection HOW DO WE FIGHT OFF DISEASE? The body has nonspecific and specific defenses against infection.

7 Nonspecific Defenses: provide protection against a wide range of pathogens involve physical & chemical barriers, fever, inflammation, interferons

8 FIRST LINE OF DEFENSE = Mechanical Barriers ● mechanical barriers / physical barriers include: -skin (and associated hairs) -mucus membranes / mucus -fluid (sweat, tears) ● as long as they remain intact, they can keep out many pathogens

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10 FIRST LINE OF DEFENSE also includes: ● CHEMICAL BARRIERS mucus – traps pathogens stomach secretions: may destroy pathogens that get swallowed

11 Chemical Barriers – cont. tears: contain the enzyme LYSOZYME (which has antibacterial action) salt in sweat: kills bacteria on the skin

12 **all other “nonspecific defenses” are considered the SECOND LINE OF DEFENSE

13 1) Inflammation produces: localized redness, swelling, heat and pain chemicals released by damaged tissues attract WBCs to the site  the mass of WBCs, bacterial cells, and damaged tissue forms a thick fluid called PUS

14 2) INTERFERONS: chemicals released by virus-infected cells; “interfere” with viral growth – slow down viral reproduction!

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16 3) Fever higher body temperature speeds up some white blood cells slows the growth of some pathogens

17 SPECIFIC DEFENSES! (“Immunity”)

18 Specific Defenses: able to distinguish “self” from “non-self” or “other” any foreign substance or cell that enters the body is inactivated or killed

19 Specific Defenses: precise / target certain pathogens also known as IMMUNITY involve specialized lymphocytes (T cells and B cells)

20 ANTIGENS… ANTIGENS: specific foreign molecules that trigger an immune response; usually located on a foreign cell’s surface

21 LYMPHOCYTES (T and B Cells) originate in the bone marrow some reach the THYMUS, where they mature into T CELLS others, the B CELLS, mature in the BONE MARROW once mature, both T cells and B cells “hang out” in the lymph nodes & spleen where they will encounter antigens

22 LYMPHOCYTE FUNCTIONS **there are two main types of lymphocyte action: 1) Humoral Immunity 2) Cell-Mediated Immunity

23 1) HUMORAL IMMUNITY ● B cells interact with antigen-bearing cells indirectly, producing the HUMORAL IMMUNE RESPONSE ● some B cells differentiate into PLASMA CELLS which produce ANTIBODIES

24 How do antibodies bind to antigen? ANTIBODIES have a specific shape that allows it to bind to specific antigen. Once antibodies have “tagged” antigen, the pathogen is “flagged” for disposal by other cells

25 HUMORAL IMMUNITY ● other B cells divide and remain around after the infection – MEMORY B CELLS ● these cells react quickly if the same pathogen returns

26 T CELLS and the CELL-MEDIATED IMMUNE RESPONSE * T cells are activated when an antigen- presenting cell displays a foreign antigen Antigen Presenting Cell (APC) antigen T cell!

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28 2) CELL-MEDIATED RESPONSE ● HELPER T CELLS are activated when they encounter foreign antigen-bearing cells ● they then divide to produce more helper T cells, which in turn go on to: -activate B cells (antibodies!) -activate cytotoxic T cells -produce memory T cells

29 T CELLS (continued) ● cytotoxic T cells: kill infected (“sick”) cells ● memory T cells: remain in the blood and respond quickly if the pathogen returns.

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31 35.3 – Fighting Infectious Disease ● PRIMARY IMMUNE RESPONSE ● SECONDARY IMMUNE RESPONSE

32 PRIMARY IMMUNE RESPONSE PRIMARY IMMUNE RESPONSE: the first exposure to an antigen  during this response, antibodies are produced for several weeks  antibodies first show up within 5-10 days  some B cells remain as MEMORY CELLS

33 SECONDARY IMMUNE RESPONSE SECONDARY IMMUNE RESPONSE: the second exposure to an antigen  rapid response due to memory cells produced during the first exposure  antibodies produced within a day or two

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35 CLASSIFICATION OF IMMUNITY 1) ACTIVE IMMUNITY ● when the person produces an immune response (including memory cells) to the antigen ● a result of direct exposure to the antigen ● long-lasting (memory cells)

36 ACTIVE IMMUNITY…  NATURALLY ACQUIRED ACTIVE IMMUNITY: person is directly exposed to the pathogen, develops a disease, gets better, & acquires immunity  ARTIFICIALLY ACQUIRED ACTIVE IMMUNITY: person receives a vaccine

37 VACCINES… **A VACCINE consists of bacteria or viruses that have been weakened or killed so they cannot cause a serious infection -includes antigens that stimulate a primary immune response but does not produce the severe symptoms of disease

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39 2) PASSIVE IMMUNITY ● person receives antibodies produced by another individual ● this is short-term only (as long as the antibodies remain in the blood) – no memory cells! ● the person remains vulnerable to the antigen if exposed at a later date

40 PASSIVE IMMUNITY  NATURALLY ACQUIRED PASSIVE IMMUNITY: fetus acquires immunity from mother through placenta and/or breast milk  ARTIFICIALLY ACQUIRED PASSIVE IMMUNITY: person receives an injection of antibodies collected from a person who has already developed immunity against a particular disease (i.e. rabies)

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42 Public Health - Prevention of Diseases Spreading 1) Regulating food and water supplies ● Cholera, Typhoid, Guinea worm

43 Public Health - Prevention of Diseases Spreading 2) Promoting vaccinations ● Herd immunity

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45 Public Health - Prevention of Diseases Spreading 3) Promoting behaviors that avoid spread of infection

46 New and Re-Emerging Diseases ● Many diseases were eliminated or were under control by the 1980s –e.g. polio and smallpox ● Over the past decade, we have had a resurgence of old diseases and introduction of new diseases –Ebola, SARS, hantavirus ● Why has this happened??

47 Reasons for New and Re- Emerging Diseases 1) Changing interactions with Animals -Human and animal habitats combine -Trade of exotic animals

48 Reasons for New and Re- Emerging Diseases 2) Misuse of Antibiotics and medications -Not following instructions on medication -Overuse of antibiotic causing resistance

49 35.4 – Immune System Disorders ● Allergies ● Autoimmune Diseases ● Attack on the Immune System (HIV / AIDS)

50 ALLERGIC REACTIONS ● triggered by antigens known as ALLERGENS ● the immune system attacks a nonharmful substance, such as pollen, pet dander, peanuts

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54 AUTOIMMUNITY / AUTOIMMUNE DISORDERS: ● the immune system fails to properly “self” & attacks the body’s own cells

55 Examples of Autoimmune Disorders:  Lupus  Rheumatoid arthritis  Type I diabetes  Multiple sclerosis

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57 AIDS  caused by retrovirus: HIV  HIV infects HELPER T CELLS  Without T H cells, the patient’s immune system stops functioning  AIDS patients become very susceptible to other infections

58 Preventing HIV Infection:  Abstinence from sexual activity / use safe practices  Don’t do intravenous drugs


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