Patho unit 4 Ch.7

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  1. Mutualism
    • Bothe the host and the microorganism benefit
    •   -e.g. E.coli, a bacterium that lives in the large intestine
  2. Commensalism
    • One organism benefits, the other is neutral 
    •   -e.g. skin bacteria
  3. Parasitism
    • One organism benefits, the other is harmed
    •   -e.g. Tapeworm, round worms
  4. Infectious Agents:
    • Ability of a pathogen to cause disease
    • Presence of enzymes, toxins, number (dosage), capsules, intracellular invasion
  5. Infectious Agents:
    • Ability of a pathogen to cause severe disease
    • Pathogens cause cellular injury because they circumvent defensive barriers
    • Pathogens directly damage cells, interfere with metabolism, and limit the functionality of the cell
  6. Infectious Agents:
    Ability to spread from one individual to another and cause disease
  7. Infectious Agents:
    • Ability of a microorganism to invade and colonize within the host
    • Produce infection
  8. Infectious Agents:
    Ability to produce toxins and influence virulence
  9. Bacteria
    • Unicellular- prokaryotic organism
    • classified as : Aerobic , and Anaerobic
    • Bacteria can live as:
    •   -Opportunists, commensals, and intracerllular and extracellular parasites
    • Produce toxins: hemolysins, leukocidins, coagulases
  10. Bacteria are characterized by their shape and size.
    Before specific culture information is available, physicians use location and appearance characteristics to begin antibiotic therapy
  11. Bacterial shape:
    • Spherical, non-motile bacteria
    • Subcategories
    •   -Diplo (pair)
    •   -Strepto (chain)
    •   -Staphylo (irregular cluster)
  12. Bacterial shape:
    • rod shaped bacteria
    • see p. 162
  13. Bacterial shape:
    • Rod shaped, rigid, spiral organisms
    • see p. 162
  14. Bacterial shape:
    • Non-rigid, spiral rods
    • i.e. siffillus 
    • See p. 162
  15. Bacterial shape:
    • Cells that do not fit in any of the other categories (i.e no defined shape)
    • No cell wall
  16. Bacterial cell wall
    • composed of peptidoglycan- a large molecular network of glucose and amino acids
    • Based on cell wall characteristics, bacteria are classified as Gram+ or Gram-
  17. Putting it together (examples of bacteria types)
    • Spherical bacteria in clusters with a thick cell wall
    •   -Gram+ staphylococci
    • Spherical bacteria in pairs with a thin cell wall
    •   -Gram- diplococci
    • Spherical bacteria in chains with a thick cell wall
    •   -Gram+ streptococci
    • "Kinda" spherical and "kinda" rod-shaped bacteria with a thin cell wall
    •   -Gram- coccobacilli
  18. Bacterial Toxins:
    Gram+ bacteria produce exotoxins
    • Exotoxins are released during its life cycle
    • Exotoxins cause specific symptoms
    • Examples: botulism, tetanus, staph food poisoning, toxic shock syndrome
  19. Bacterial Toxins:
    Gram- bacteria produce endotoxins
    • Endotoxins are released during cell death
    • Produce generalized symptoms 
    • Example: salmonella food poisoning
  20. Sporulation
    • The formation of endospores
    • Produced when conditions are unfavorable
    • Endospores help the chromosomal contents of he bacteria survive extreme temperatures, radiation, and harsh chemicals
    • Once optimum conditions return, the spores will germinate
  21. Viruses
    • A virus is not technically living 
    •   -it has no metabolism
    • Obligate intracellular parasite
    • The virus provides the RNA and DNA replicate, and the host cells provide the energy and resources
    • Components include nucleic acid, capsid, and an optional envelope
  22. Viral Replication
    • Depends on :
    •   -Absorption
    •   -Penetration
    •   -Uncoating
    •   -Replication
    •   -Assembly
    •   -Release new virions
  23. Fungi
    • Important to the decomposition and recycling of organic material
    • Fungi are divided into two groups, yeasts and molds
    •   -Candida ablicans (yeast infection)
    •   -Tinea corporis (ringworm)
    • Fungi release mycotoxins and enzymes that damage connective tissues
    • Diseases caused by fungi are called mycoses
    • Fungi can cause superficial and deep infections
    • Some Fungi are part of the normal body flora and act as opportunists
  24. Immunodeficiencies
    • Usually manifested by the tendency to develop unusual or recurrent infections
    • Occur because of the impairment of one or more components of the immune or inflammatory system
  25. Primary immunodeficiencies
    • Occurs during Leukocyte development in the fetus or embryo
    • Can effect one or more white cell lines
    •   -The number of cells affected dictates the degree of the deficiency
    •   -If the T and B cell lines are affected, the patient will have normal number of they other leukocytes, but they will have low number of the lymphocytes, and diminished levels of antibodies
  26. Primary Immunodeficiencies:
    Di George syndrome
    • Partial or complete lack of the thymus
    • Patient demonstrates lymphopenial and decreased t cell function
  27. Primary Immunodeficiencies:
    Burton's Agammaglobulinemia Syndrome
    Failure of early B cells to become mature B cells
  28. Primary Immunodeficiencies:
    Wiskott-Aldrich syndrome
    • X-linked recessive dissorder
    • IgM production is depressed
  29. Primary Immunodeficiencies:
    Selective IgA deficiency
    • produce other types of antibody but not IgA
    • Can cause chronic intestinal candidiasis
    • Increased allergen uptake and more severe allergic responses
  30. See Immunodeficiencies slide on p. 166
  31. Acquired Immune Deficiencies:
    Secondary Immunodeficiencies
    • Nutritional deficits
    • Chemotherapeutic agents 
    • Coticosteroids
    • Burn victims
    • Emotional stress
    • Others: pregnancy, infancy, infections, malignancies, aging, diabetes, anemia
  32. Graft-Versus-Host Disease (GVHD)
    • T cells in transfused blood or bone marrow transplants can be immunologically active, therefore capable of cell-mediated immunity
    • Recipients cells are not immunologically active, or they don't have any, so they can't fight back
  33. Retrovirus
    • infect cells by binding to a surface receptor and inserting their RNA into the target cell
    • A viral enzyme, reverse transcriptase converts the RNA to DNA and inserts the viral genetic material into the target cell DNA
    • The genetic material can begin replicating immediately or remain latent for a period of time
    • e.g. HIV
  34. Human Immunodificiency Virus (HIV)
    • spread primarily through contact with blood or body fluids containing the virus. It is also speculated the lesions from other sexually transmitted diseases provide opportunities for the virus to enter the host
    • Concentrations of HIV
    •   -high: blood and semen
    •   -Low: vaginal fluid, tears, sweat, breast milk
    • Has also been transmitted through infected tissue transplants
  35. AIDS Pathophysiology
    • Virus has a gp 120 protein which binds CD4 receptor
    • Therefore, HIV infects mainly CD4+ (helper T) cells 
    • The number of CD4+ cells continues to diminish until patient is prone to opportunistic infections
  36. Testing for HIV
    • Window period
    •   -Lag time between infection and detection
    •   -Currently about 7 days
    • Antigen and antibody tests for screening and confirmation
    • Count CD4+ cells
  37. Treatment for HIV
    • Since 1996, Highly active antiretrovial therapy (HAART)
    •   -Three synergistic drugs
    • Drugs can be 
    •   -entry inhibitors
    •   -Reverse transcriptase inhibitors (NNRTIs)
    •   -Integrase inhibitors
    •   -Others
    • HIV vaccine
  38. Hypersensitivity
    • Inappropriate immune response that results in damage to the host
    •   -Allergy: hypersensitivity to antigen from environment 
    •   -Autoimmunity: hypersensitivity to antigen from self
    •   -Alloimmunity: hypersensitivity to antigen from donor
  39. Types of Hypersensitivity
    • Type I
    •   -IgE-mediated 
    • Type II
    •   -Tissue specific
    • Type III
    •   -Immune complex-mediated
    • Type IV
    •   -T cell-mediated -non antibody
    • Almost all types will overlap to some degree
  40. Type I:
    Immediate hypersensitivity
    • Mast cell-bound IgE antibody reacts with antigen and stimulates mast cell degranulation
    • Some individuals have an inherited tendency to respond to allergens with continual production of IgE
    •   -1 parent with allergy-40%, 2 parents-80%
    • Symptoms: Allergic rhinitis, asthma, urticaria, anaphylactic chock, diarrhea, and /or vomiting
  41. Type II:
    Tissue-Specific Hypersensitivity
    • Free antibody (IgG or IgM) reacts with cell-surface antigens 
    •   -Activates phagocytosis and complement
    • Examples of Type II
    •   -Transfusion reactions
    •   -Hemolytic disease of the newborn
    •   -Autoimmune thyroiditis
    •   -Autoimmune glomerulonephritis
  42. Type III:
    Immune Complex Hypersensitivity
    • Antibody reacts with free, soluble antigen to form complexes that precipitate in the tissues
    • When soluble antigen combines with antibody, complexes precipitate out of the plasma and deposit in tissues, bind/activate complement, and cause tissue damage
  43. Examples of Type III
    • Autoimmune diseases
    •   -Lupus
    •   -Rheumatoid arthritis
    • "Farmers Lung"
    •   -Hypersensitivity to inhaled allergens in dairy farmers
    • Glomerulonephritis
    •   -
  44. Type IV:
    Delayed Hypersensitivity 
    Cell-Mediated Hypersensitivity 
    Contact Hypersensitivity
    • Sensitized cytotoxic T cells attack tissues
    • Sensitized helper T cells release lymphokines that recruit macrophages 
    • Antibody and complement not directly involved
    • Symptoms delayed for 48-72 hours
  45. Examples of Type IV delayed Hypersensitivity
    • Poison ivy, poison oak, topical drugs, soaps, perfumes, sutures... really any chemical substance (many acting as haptens) including metals like nickel in cheap jewelry
    • Process takes days but effects can last for years (blisters, peeling, weeping
    • TB skin test and acute transplant rejection are examples.
  46. See 7-9 slides on p.171
  47. Self vs Non-Self Recognition 
    (Immune Tolerance)
    • If billions of gene combinations are made, each capable of binding to its specific molecular shape, then it is critical to remove from the body those which bind to the body's own tissues
    • this is called self/non-self recognition or tolerance
    • T cells are tested in the thymus
    •   -97% "fail" the test and die via apoptosis
    •   -3% "pass" and are allowed into circulation
    • B cells are tested in the bone marrow
  48. Autoimmunity
    • a breakdown of tolerance in which the body's immune system begins to recognize self-antigens as foreign
    • Common origin
    •   -Autoimmune diseases result from a genetic predisposition and a hypersensitivity to and environmental stimulus.
  49. Common Auto immune Diseases
    • There is one or more for every system of the body
    • Graves disease (thyroid)
    • Hashimoto thyroiditis
    • Type I (Insulin dependent) diabetes mellitus (pancreas)
    • Multiple sclerosis (myelin sheath in nervous system)
    • Rheumatoid arthritis (joints)
    • Myasthenia gravis (ACh receptors)
    • Goodpasture syndrome (kidney-glomerulus)
    • Autoimmune thrombocytopenia (platelets)
    • Pernicious anemia (parietal cells of stomach)
  50. Autoimmiunity:
    Systemic Lupus Erythematosus (SLE)
    • Chronic, systemic inflammatory disease
    • Production of a variety of antibodies: nucleic acid (98% of patients), erythrocytes, phospholipids, and histone proteins
    • Positive anti-nuclear antibody (ANA) test
    • Circulating immune complexes deposit in tissue, especially the glomerular membrane
    • "Lupus"(wolf-like), photo-sensitive "red" facial rash
  51. Symptoms of Systemic Lupus Erythematosus
    • Arthritis -90%
    • Vasoculitis and rash - 70-80% (discoid lupus)
    • Renal disease - 40-50%
    • Anemia - 50%
    • Cardiovascular disease - 30-50%
  52. Graft Rejection
    • Alloimmunity occurs when and individual's immune system reacts against antigen of other members of the same species
    • Transplants are complicated by an alloimmune response to donor HLA antigens
    • Classified as hyperacute, acute, or chronic depending on activation time
  53. Graft Rejection:
    • Patients have preexisting IgG or IgM antibody to the tissue
    • Antibody binds to the tissue and activates an inflammatory response
    •   -type II hypersensitivity 
    • This results in the cessation of blood flow to the graft  - "white graft"
    • Pre-transplant testing minimizes this risk
  54. Graft Rejection:
    • The rejection is cell mediated and occurs approximately 2 weeks after the transplant 
    •   -Type IV hypersensitivity 
    • Immunosuppressive drugs try to minimize this response
  55. Graft Rejection:
    • Can occur after months or years of normal function
    • Reaction to minor HLA antigens
    • No matter how much the immune response is suppressed, the tissue is still foreign
    • Signs and symptoms
    •   -Slow, progressive organ failure and damage to endothelial cells of the blood vessels
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Patho unit 4 Ch.7
2013-10-16 20:46:34
Patho unit

Patho unit 4 Ch.7
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