ANSC 100

  1. iClicker Q
    Which accuratly describe on of the duties of the ABVMA?
    a) Vet licensing exams
    b) writes laws and sets minimum standard
    c) acredits vet programs
    d) apply punitive measures to vets not meeting min standards
    • a) Vet licensing exams CVMA role
    • b) writes laws and sets minimum standard governments role
    • c) acredits vet programs CVMA role
    • d) apply punitive measures to vets not meeting min standards
    • ABVMA sets policies higher than minimum standards
  2. What are the elements of small pox?
    • -debilitating diseseas- 40% mortality
    • -leading cause of blindness
    • -blamed for wiping out Native New World civilizations
    • -killed up to 0.5 M Europeans per yr in the end of the 18th C
    • -in 1967 WHO estimated 15M contracted and 2M died/year
    • -Declared eradicated in 1979!!!
  3. Which was on of the few diseases to be eradicated and when? Why was it eradicated?
    • Small Pox
    • ~>175 years
    • declared eradicated in 1979
    • Eradicated due to vaccination and quarantine together
  4. In the 10th C how were small pox dealt with?
    • -"variolation" was used = scratching skin with small amounts of pus from smpox scabs or blowing material into nostrils
    • -Goal= mild infection and then immunity
    • -however patients sometimes got full blown small pox
    • -some ppl observed that infection with cow pox seemed to prevent small pox
  5. Who invented to first  vaccination developed form a disease shared btwn animal and human (cow pox) and in what year?
    -1976: Edward Jenner, MD in England
  6. What did Edward Jenner Hypothesis and do?
    • -Hypothesifecting: he could prevent smallpox by infecting someone with cowpox
    • -May 13 1796- inoculated 8yr old James Phipps (son of Jenners gardener) with a cowpox blister from milkmaid Sarah Nelmes (who had caught it from Blossom the cow) He then exposed james to smallpox, who did not catch it = called it a VACCINATION
  7. What is the science behind Smallpox vaccination by Edward Jenner?
    • -known: small pox is more dangerous than "variolation" and cowpox less dangerous than "variolation"
    • -Hypothesis: Infection with cowpox gives immunity to smallpox
    • -Test: If variolation after infection with cowpox fails to produce a smallpox infection, immunity in smallpox has been achieved
    • Consequence: Immunity to smallpox can be induced much more safely that by variolation
  8. What happened with small pox in St.Johns Newfoundland (what year?)?
    • -Newfoundland= worlds first mass vaccination
    • -1800
    • -Dr. John Clinch (medical missionary and classmate of Jenner) wrote to Jenner to get vaccine
    • -over 700 people vaccinated in Trinity St. Johns and Bonavista by 1801
  9. How was smallpox eradicated? How long did it take?
    • -Small pox took over 175 years to eradicate through vaccinations and aggressive epidemiology and quarantine response to outbreaks
    • -(cow pox was replaced by vaccinia virus in the 1900's)
  10. Who was the immunology pioneer and what did he do?
    • -Louis Pasteur
    • -if fresh p.m was given to normal chicken =dead chicken
    • -however if inserted normal chicken with Aged p.multocida =no disease or death
    • -then inserted fresh p.multocida into that surviving chicken =no dease or death
  11. Why would you weaken a pathogen and then insert it in an animal?
    -If weaken pathogen --> give immune system time to figure out what to do and gain immunity (so if inject with fresh after it won't die)
  12. What did Louis Pasteur figure vaccines out for?
    • Anthrax and Rabies
    • -Grew Anthrax at a high temp and made them avirulaent
    • - these "attenuated" (damaged because of hight temp) bacteria were used as a vaccine in sheep
    • -The vaccine protected the sheep from infection by virulent form (unvaccinated ones died)
    • -Used similar methods and developed a Rabies vaccine using dried up spinal cord from rabies-infected rabbits
  13. Whats the history of Anthrax and Rabies?
    • Anthrax:
    • -Livestock and humans working with them and their products (sheep,skins) were killed
    • Rabies
    • -Dogs, wolves, many others. Killed livestock and many people
  14. Where was immunity at by 1900?
    • -Existence of immunity to infectious diseases of animals was well recognized
    • -Bacteria were being ID and classified
    • -Vaccines against tetanus, rabies, and other diseases existed
    • -"viruses" were still unknown - a "filterable particle" (knew that something in animals caused disease and were transmissible)
    • -Before antibiotics vaccines were thoguht to be the solution to most infections, if they could be developed
  15. iClicker Q
    When pasteur treated chickens with fresh m =sick and died
    If treated with aged and gave and then gave fresh = no death
    What does this illustrate?
    It illustrated that treatment with "attenuated" bacteria allowed the development of immunization
  16. DEFINE
    • Any deviation from, or interuption of, the normal structure or function of any body part, organ or system
    • (- manifested by characteristic set of symptoms and signs
    • -Etiology, pathology and prognosise may be known or unknown)
  17. What is the difference between syndrome and disease?
    • Disease: Any deviation from, or interuption of, the normal structure or function of any body part, organ or system
    • Syndrome: a set of symptoms occuring together , a symptom complex (can call it a syndrome before we know what diseases causes it)
    Pathogen or Pathogenic agent
    • -An agent of microorganism possessing the ability to cause a disease in a given animal in a given environment
    • Examples: infectious organisms (sometimes carcinogens, toxins)
  19. Primary Pathogen and Opportunistic Pathogen
    • -Primary Pathogen - causes disease nearly ever time it invades a healthy animal, even in low numbers
    • -Opportunistic Pathogens- low virulence and causes death only if administered in high doses or immune defenses are impaired
  20. Define Pathology
    Study of the events and reactions particularly changes in body tissues and organs, occuring in the development of disease (pathogenesis)
  21. Define pathogenesis
    the whole course a disease takes, what happens
  22. Define Etiology
    the determination and study of the factors that contribute to the production of a diseas (ie pathogens plus enviro)
  23. Define Diagnosis
    determination of the nature of a case of a disease (NOTE doesnt necessarily require determination of etiology)
  24. Define Prognosis
    a forecast of the probable course and outcome of a disease
  25. Define Pathogenicity
    the quality of producing or the ability to produce pathologic changes or disease
  26. Define Virulence
    the degree of pathogenicity of a microorganism, as determined by case fatility rates abd/or its ability to invade the tissues of the host, evade body's defenses and cause disease (pathogenicity with measurements attached)
  27. Define Antigen
    Any foreign substance (protein etc...O that can bind to specific lymphocyte receptors and so induce an immune response (ie allergy)
  28. Define Antibody
    the immunoglobulin molecule synthesized on exposure to an antigen, which can combine (attach) specifically with that antigen
  29. Describe Primary defenses against Infectious disease
    • Purpose is to impair entry of microorganisms through the epithelium into the bodyn (so part of process but not  immune system itself)
    • -physcial barriers
    • -innate immunity
  30. Describe Secondary Defenses against infectious disease
    • Purpose is to deal with microorgansims that gain entry into body and escape primary defenses
    • -acquired immunity
  31. What is aquired immunity?
    • Secondary defense
    • -antibody production (humoral immunity)
    • -cell mediated immunity
  32. Give examples of each of these steps
    Invading microorgansims -->
    Physical barriers (primary)--->
    Innate Immunity (primary)-->
    Acquired Immunuty (secondary)
    • Invading microorgansims
    • -->Physical barriers (primary) ie skin, self cleaning, normal flora
    • --->Innate Immunity (primary) ie inflammation, lysozyme
    • -->Acquired Immunuty (secondary) ie antibody production, cell-mediated immunity
  33. What does the primary defense mechanism "skin" do
    • -barrier to penetration, as long as it is intact
    • -physical injury often opens up entry of microorganisms
    • -skin carries a dense, stable resident bacterial flora
  34. What is the role of the "respiratory tract" as a primary defense mechanism?
    • -lined with cilitated epithelium, and mucus secreting cells (goblet cells)
    • -provides mucus layer atop moving cilia (traps dust)
    • -traps microbes and particles carrying microbes
    • -mucus has "antiseptic" properties due to lgA and lysozyme (toxins kill bacteria) action
    • -cilia beating transport these particles out of the respiratory tract- up the "mucociliary escalator" to the pharynx then swallowed
    • -coughing- expulsion of large particles to get rid of invadors
  35. What is the role of the "Gastrointestinal tract" as a primary defense mechanism?
    • -gastric juices act as excellent bactericide due to acidity
    • -GI mucins- glycoproteins secreted into the intestine, form a mucous gel
    • -Mucous gel serves as a barrier keeping pathogens and chemicals away from the enterocytes, acts as a lubricant, blocks chemical insults, traps and expels pathogens
    • -bacteria that enter the small intestine are trapped in mucus film covering epithelium
    • -inner layer of mucus is rich in defensins and lysozyme that helps destroy bacteria
    • -mucus is transported out of the body with feces
    • -normal resident population of bacteria in large intestine usually help to prevent overgrowth of pathogenic bacteria (and are vital in digestion) unless resident population decreased
  36. iClicker Q
    The primary immune system of the respiratory tract includes...
    Mucus with lysozymes that has antiseptic properties: coilia and coughing
  37. Give examples of (primary) physical barriers
    skin, self cleaning, normal flora
  38. Give examples of innate immunity (primary)
    inlfammation, lysozyme
  39. Give examples of acquired immunity (secondary)
    antibody production, cell-mediated immunity
  40. What is/are the primary immunity?
    physical and innate immunity- always on
  41. What is/are the secondary immunity?
    acquired immunity -Turned on by antigens
  42. Compare Innate and acquired immunity in terms of these characterisitics:
    cells engaged, evolutionary history, onest, specificity, potency, memory, effectiveness
    • cells engaged: I= macrophages, dendritic cells. neutrophils, NK celss.      A= T and B cells
    • Evolutionary history: I= ancient, A = Recent
    • Onset: I= rapid(min to hrs), A= slow (days-weeks)
    • Specificity: I= common microbrial structures, A= Unique antigens
    • Potency: I=May be overwhelmed, A= rarely overwhelmed
    • Memory: I=none, A= significant
    • Effectiveness: I=does not improve, A=improves with exposure
  43. What is the relationship between physcial barriers, innate immunity and acquired immunity?
    • (graph)
    • Surface barriers provide emmediate protection. innate mechanisms provied immediate protection that keeps microbrial invaders at bay until acquired immunity can develop. Acquired immunity may take several days or weeks to become affective.
  44. Does acquired immunity improve?
    with exposure
  45. What kind of immunity is inflammation?
    innate immunity
  46. How does inflammation occur with exposure to microbrial invasion, trauma, heat, and chemicals?
    • results in tissue damage- releasing alarmins &/or
    • toll-like receptors that recognise pathogen-associated molecular patterns (PAMPS which recognise generic bacteria) which are highly conserved molecules (such as lipopolysacchardies or lipoteichoic acids) that are found on many different organisms
    • TLRs or Alarmins trigger innate immune defenses of sentinel cells-result = inflammation
    • vassoactive molecules  (vessels expand) or cytokines are released, activation vascular changes, phagocytic cell activity, and systemic responses
    • these activate neutrophils  and macrophages, resulting in the killing of bacteria and tissue repair process
    • (graph drawn in book)
  47. Does inflammation mean infection?
  48. *What are the 5 classical signs of inflammation?
    • redness (rubor)
    • heat (calor)
    • pain (dolar)
    • swelling (tumor)
    • loss of function (functio laesa)
  49. What is the terminology at the end of the word to indicate inflammation>?
  50. Compare "acute" vs "chrponic"
    • acute: sudden onset, short duration, does not imply severity, may be mild or severe, started recently and came on fast
    • chronic: onset is slow, long lasting, often results in impaired function, may begin with acute episode that does not resolve or recurs (condition to deal with over time)
    • note both can be severe
  51. For secondary defenses (acquired immunity) the ummune system involves which two types of cell immunity?
    cell-mediated and humoral immunity
  52. What is the difference between cell-mediated and humoral immunity?
    cell mediated= no antibodies and humoral= involves antibodies
  53. What are the 5 major components of the acquired immune system?
    • 1. Cells that trap and process antigen and then present in for recognition of the immune system
    • 2. Cells that have receptors for the processed antigen. These cells can bind and respond to the antigen (antigen-sensitive cells).
    • 3. cells that, once activated by antigen, will produce specific antibodies, or will participate in the cell-mediated immune responses against the antigen (effector cells)
    • 4. Cells that will retain the memory of the vent and react rapidly to that specific antigen if it is encountered at a later time
    • 5. Cells that regualte this response and ensure that it functions at an appropriate level (inhibit immune responses)
  54. In cell-mediated immunity which type of cells form an essential part of the secondary defenses?
    WBC (leukocytes): Granulocytes and mononuclear cells
  55. What are granulocytes
    neutrophils, eosinophils (consume bacteria), basophils, which adhere to, engulf, and digest foreing particles
  56. What are mononuclear cells (lrg)
    • WBCs involved in the secondary defenses
    • monocytes- phagocytic: engulf foreign materials, promote the immune response
    • lymphocytes (T-cells)-not phagocytic: signaling, cytotoxic (killer) cells
    • also lymphocytes (B-celss)- antibody production (humoral immunity), memory cells
  57. What is humoral immunity?
    the antibody response
  58. what are antibodies
    soluble antigen receptors
  59. *what are antibody proteins known as?
  60. what are the 5 types of immunoglobulins in mammals?
    IgG, IgM, IgA, IgE, IgD
  61. What cells produces antibodies?
    produced by B-cells: a type of lymphocyte
  62. What are antibodies specific too?
    particular invading material- the antigen
  63. What must an antigen be recognised as for an antibody response (humoral immunity)
  64. when must antigen receptors reliably bind foreign antigens?
    on their first encounter
  65. how do antibodies bind to almost any invading microorganism?
    by scrambling and rearranging the peptide sequences that comprise the antigen-binding site (millions of conformations)
  66. How does humoral immunity (anitbody response) occur?
    • initial invasion (infection) stimulates production of proteins called "antibodies" by plasma cells (a type of lymphocyte)
    • antibodies bind specifically to antigen and hasten its destruction or elimination by various types of lymphocytes and other cells and their products
    • stimulates production of "memory" cells to initiate a quicker and larger response the next time the antigen is encountered
  67. Describe active versus passive immunity
    • Active:
    • immunity is produced by the body
    • in response to an administration of an antigen
    • Triggers the body's immune response (and memory)
    • (better immunity that lasts longer)
    • *body develops own immunity and own response
    • Passive:
    • protection of individual by administering antibodies produced in another individual (ie transfusion and colostrum)
    • no immune response triggered to the antigen in the recipient
    • no memory
  68. what is the role of cholostrum
    cholostrum is high in antibodies and so the baby takes in the proteins- after 24 hours the stomach lining stops taking in proteins
  69. What is active immunity. Explain the factors and the disadvantages and advantages
    • *exposure to, or vaccination with love attenuated or dead infectious agents to produce an immune response
    • exposre to antigen causes aniaml to mount a protective immune respnse that may be antibody or cell mediated or both
    • Reimmunization or exposure to infection results in a secondary immune response
    • disadvantage: protection is not conferred immediatly, often requires "boosters"
    • advantage: once estb immunity is long-lasting and capable of re-stimulation
  70. Describe passive immunity
    • production of temporary immunity by administering of preformed antibodies from a resistant to a susceptible animal.
    • -gives immediate protection
    • -antibodies are gradually broken down and immunity wanes
    • can block the development if active immunity until the passive immunity drops off. EX: neonatal consumption of colostrum milk; antiserum to tetanus "tetanus antitoxin"
  71. If the attenuated bacteria are in the body but dont grow the body cant react much so you add ____?
    Adjuvent (immune stimulant put in vaccine to make it more affective)
  72. For vaccination (immunisation) what are the many routes that have been successfully used?
    • intramuscular injection
    • subcutaneous injection (majority of modern injectables)
    • oral (rabies in wild carnivores, polio)
    • intranasal (IBR in cattle, "kennel cough" in dogs)
    • eyedrops (feline infectious peritonitis- corona virus)
Card Set
ANSC 100
Three Immunity Lectures