Microbiology Lecture Week 3

  1. The body has the ability to defend itself from invasion by anything foreign - be it a
    • Molecule
    • Cell
    • Organism
    • Organ
  2. In general, immunity constitutes all the physiological mechanisms which allow the body to recognize materials as
    foreign or abnormal and to neutralize or eliminate them
  3. Natural barriers– Inflammation are what type of immunity
    Innate Immunity
  4. Antibodies– T-cell response are what type of Immunity
    Specific or Adaptive Immunity
  5. Describe Inflammatory responce
    nonspecific: where the specific identity of the invader is not needed
  6. Describe classical immune response
    specific: where the specific identity of the invader initiates there sponse that is mediated by lymphocytes
  7. Physical Barriers
    • Tightly associated epithelial cells including skin and membranes lining thegastrointestinal, genitourinary and respiratory tracts
    • Cells ‘slough’ off and are replaced – can also remove adherent bacteria
    • Cells ‘slough’ off and are replaced – can also remove adherent bacteria
  8. Biochemical Barriers
    synthesize substances that trap or destroy microorganisms
  9. Name synthesize substances that trap or destroy microorganisms
    • Perspiration, saliva, tears and earwax (cerumin) are all biochemical secretionsthat trap potential disease causing micorganisms
    • Perspiration, tears and saliva contain lysozyme that attacks cell walls of grampositivebacteria
  10. Immune responses can be classified as:
    • nonspecific: (inflammatory response)
    • specific: classically called the immune response
  11. Rapid response is Innate response or Adaptive response
    Innate response
  12. Slow response is Innate response or Adaptive response
    Adaptive response
  13. Innate Immunity Purpose
    Alert other innate and adaptive immune cells to pathogen presence; directlly kill pathogen; encorage the development of an adaptive immune responcse
  14. Addaptive Immunity Purpose
    Assist in efficacy of innate immune responce; produce highly specific ligands for pathogens
  15. Innate Immunity cellular components
    Macrophages, dendritic cells, granulocytes, mast cells, natural killer cells
  16. Adaptive Immunity Cellular components
    • T cells
    • B cells
  17. The innate immune system (non-specific) is characterized by
    physiologic barriers to entry ofpathogenic organisms and very fast host defense responses.
  18. The adaptive immune system (specific) consists of
    cells displaying antigen recognitionmolecules and has the capacity for long-term memory
  19. What IMMUNITY serves to protect the host without prior exposure to an infectious agent—i.e., before specific or adaptive immunity has had a chance to develop.
    Innate Immunity
  20. What immune system does not confer long-lasting immunity to the host but rather provides immediate defense against infection.
    Innate immune system
  21. First Line of Defense
    Physical and Biochemical Barriers:
  22. Physical Barriers
    • Tightly associated epithelial cells
    • skin
    • membranes lining thegastrointestinal
    • genitourinary
    • respiratory tracts
  23. Biochemical Barriers
    • Perspiration
    • saliva
    • tears
    • earwax (cerumin)
  24. all biochemical secretionsthat trap 
    potential disease causing micorganisms
  25. Perspiration, tears and saliva contain
    Lysozyme that attacks cell walls of gram positive bacteria.
  26. Second line of defense
  27. A vascular, non-specific, immediate, response to cellular injuryor invasion
    Brings in tools to isolate, destroy and remove damaged tissueand infectious material
    Provides the foundation for healing
    Inflammation:Second line of defense
  28. Vascular Response
    • Blood vessel dilation
    • Increased vascular permeability and leakage of fluid out of thevessel
    • White blood cell adherence to inner walls of vessels and their migration through vessel walls to the site of injury
  29. Key players in theacute inflammatory response
    • Cells
    • Soluble protein systems
  30. Key players in theacute inflammatory response
    • mast cells
    • capillary endothelial cells
    • Neutrophils, Eosinophils, Basophils
    • Macrophages – activated monocytes
  31. Key players in theacute inflammatory response
    Soluble protein systems
    • cytokines
    • proenzyme soluble (plasma) protein systems
    • - Complement system
    • - Clotting system
    • - Kinin systemsPro-enzyme
  32. Three plasma protein systems are essential to an effective inflammatory response:
    • – Complement system
    • – what will be emphasized in class
    • – Clotting system– Kinin system
  33. Some of the proteins are enzymes (proenzymes) that are activated by
    products of cell damage or infection
  34. An active enzyme subtrate complex consist of
    Positive modulator and a Subtrate 
  35. Complement system consists of several
    plasma proteins (Cproteins) that constitute the complement system: represents10% of circulating serum protein
  36. Activation of complement cascade can destroy
    pathogens directly, and canactivate and/or collaborate with all other components of the immuneresponse
  37. Activation of complement system can be accomplished asfollows:
    • Classical pathway
    • Lectin pathway
    • Alternative pathway
  38. Classical pathway:
    activated by proteins of acquired immunity (specific/adaptive) such as antibodies bound to antigen
  39. Lectin pathway:
    activated by certain bacterial carbohydrates
  40. Alternative pathway:
    activated by gram-negative bacteria and fungal cell wall polysaccharides (complex carbohydrate)
  41. activated by antibody-antigen complexes
    A. Alternative pathway
    B. Lectin pathway
    C. Classic pathway
    C. Classic pathway
  42. Activated by mannose-binding lectin(carbohydrate patterns present on surface of bacterium)

    C.  Lectin pathway
  43. activated by gram negative bacteria and fungal wall polysaccharides
    A. Alternative pathway
    B. Lectin pathway
    C. Classic pathway
    A. Alternative pathway
  44. Complement Plasma Protein System activated by presence of
  45. Activated by presence of antigen-antibody complexes
    A. Alternative pathway
    B. Lectin pathway
    C. Classic pathway
    C. Classic pathway
  46. Activated by presence of pathogen products, endotoxin
    A. Alternative pathway
    B. Lectin pathway
    C. Classic pathway
    A. Alternative pathway
  47. Activated by presence of carbohydrates on surface of bacteria

    C.  Lectin pathway
  48. Contributions to inflammation:
    • liberate histamine (C3a, C5a)
    • increase endothelial cell adhesion (C5a)•
    • neutrophil chemotaxis (C5a,C345)
    • increase bacteria susceptibility to phagocytosis (C3b)
    • breaks down microorganism cell membranes (C5b-9)
  49. There are at least 11 TLRs, each
    specific for detecting differentbiologic classes of molecules.
  50. Cellular Mediators of Inflammation
    • Granulocytes = Neutrophils– Eosinophils– Basophils
    • Other blood components = Monocytes (precursor to macrophages– Platelets– Mast Cells– Natural killer cells
  51. Mast Cells
    • Central cell in inflammation
    • Originates in bone marrow
    • Cellular bags of granules located in close connective tissueclose to blood vessels– Found in skin and linings of GI and respiratory tracts
  52. Causes of Mast cell activation:
    • Physical injury
    • Chemical agents
    • Immunologic activation usually resulting from complement activation or presence of antibodies
    • Activation of toll-like receptors by bacteria and viruses
  53. Non-granular made in the
    lymph nodes
  54. Granular made in the
    bone marrow
  55. most common WBC. Protect against infection, involved in inflammation

    A. Neutrphil
  56. WBC with polymorphicnuclei--destroy parasitic organisms--involved in allergic reactions

    B. Eosinophil
  57. infrequent WBC cell (1%)--essential to non-specific immunity--release histamine that dilatesblood vessels

    B. Basophil
  58. the main effector cell in acute inflammation
  59. move toward area of tissue damage via chemotaxis and expressadhesion molecules on vascular endothelium = “CAM’s”
    short-lived and need constant replenishing
  60. contain large numbers of lysosomal cytoplasmic granules rich inproteolytic enzymes
    As they die, continue to release proteases–
    Arrive at an injury site first
    A. Neutrophils
    B. Macrophage
    A. Neutrophils
  61. break down and eradicate damaged tissue
    destroy bacteria
    tag as antigens and activate the adaptive immune response
    Produce pro-inflammatory cytokines (middle-man)
    A. Neutrophils

    B. Macrophage
    B. Macrophage
  62. Similar to mast cells in content of granules
    Source of IL-4 (Interleukin-4)
       – Key regulator of acquired immune response
       – Associated with allergies and asthma

    A. Basophil
  63. Fever enhances the immune response by
    speeding upmetabolism and phagocyte activity
  64. Acts as mechanical barrier
    Keratin layer of intact skin
  65. Lysozyme in tears and other secretions (mode of action)
    Degrade peptidoglycan in bacteria cell wall
  66. Fever 
    • 1. A macrophage ingest a gram negative bacterium
    • 2. The bacterium releases endotoxins that induce macrophage to produce cytokines(IL-1 & TNF)
    • 3. Macrophages release cytokines into the bloodstream  that travel to the hypothalamus of the brain
    • 4. Cytokines induce the hypothalamus to produce protaglandis which reset the body thermostat to higher temp producing fever
  67. Keratin layer of intact skin asct as 
    a mechanical barrier
  68. Low pH in stomach and vagina; fatty acids in skin retards gorwth of 
  69. Respiratory cilia elevate 
    mucus containing trapped organisms
  70. Surface phagocytes (e.g., alveolar macrophages) ingest and 
    destroy microbes 
  71. Normal flora of throat, colon and vagina occupy receptors which 
    prevent colonization by pathogens
  72. NKC limit growth of microorganisms within the body by 
    killing virus infeted cells
  73. Neutrophils limit growth of microorganisms within the body by 
    Ingest and destroy microbes 
  74. Macrophages and dendritic cells limit growth of microorganisms within the body by 
    Ingest and destroy microbes and present antigen to helper T cells 
  75. Interferons limit growth of microorganisms within the body by 
    Inhibit viral replication 
  76. Fever limit growth of microorganisms within the body by 
    Elevated temperatures retards bacterial growth 
  77. Inflammatory response limit growth of microorganisms within the body by 
    Limits spread of microbes 
  78. innate immune system (non-specific) is characterized by
    physiologic barriers to entry of pathogenic organisms and very fast host defense responses
  79. adaptive immune system (specific) consists of
    cells displaying antigen recognition molecules and has the capacity for long-term memory
  80. The cellular and humoral responses are not
    Not independent
  81. Humoral immunity
    • B-cell antibody mediated
    • – “Fluid” immunity
    • – Circulating antibody
  82. Cell-mediated immunity
    T cell differentiation
  83. Antibodies or T cells produced after either a natural exposure to anantigen or after immunization name this IMMUNITY
    Active immunity
  84. Preformed antibodies or T lymphocytes are transferred from adonor to a recipient name this IMMUNITY
    Passive Immunity 
  85. Invasion by foreign (non-self) molecules are
    • proteins
    • carbohydrates
    • nucleic acids
    • foreign particles
    • cells like viruses, bacteria , blood cells, etc.
  86. The response largely comes into play once an invader has
    penetrated the skin and made its way into the circulatory system
  87. The immune system is capable of distinguishing "self " from"non-self " this ability is acquire during 
    embryonic development
  88. What is embedded in the membranes of all of our own cells that identifies a cell as a self cell
    Histocompatibility complex (MHC) is a glycoprotein 
  89. Lymphocytes and phagocytes interact to cause four definingcharacteristics:
    • – Self/non-self recognition
    • – Specificity
    • – Diversity
    • – Memory
  90. Self versus non-self recognition
    Each kind of cell or virus has a unique identity that is distinct from the host
  91. MHC (major histocompatability complex) markers ia a 
    Plasma membrane self-recognition proteins
  92. T cell receptors (TCRs) are antigen receptors that ?
    recognize MHC markers as self, antigens as non-self
  93. Specificity defenses are tailored to
    target specific antigens
  94. Adaptive immune system has the capacity to remember an 
  95. If adaptive immune system encounters the same antigen again
    B and T cells make a faster,stronger response
  96. Immunogenic:
    capacity of an antigen to elicit an immune response
  97. How do some pathogens escape detection 
    The mimic self antigens
  98. Once a B or T cell recognizes and binds to a specific antigen, itbegins to divide by
    • mitosis
    • – All descendent cells recognize the same antigen
  99. T cells do not recognize an antigen unless it is presented by an
    antigen-presenting cell (APC)
  100. Macrophages, B cells, and dendritic cells digest particles and
    display antigen-MHC complexes
  101. Effector cells
    – Differentiated lymphocytes (B and T cells) that act at once to fight infection
  102. Memory cells
    – Long-lived B and T cells reserved for future encounters with thesame antigen
  103. Antibody-mediated immune response
    B cells produce antibodies that bind to specific antigen particles in blood or interstitial fluid
  104. Cell-mediated immune response
    Cytotoxic T cells and NK cells detect and destroy infected oraltered body cells
  105. T cells perform several important functions, which can bedivided into two main categories named
    • The regulatory functions are mediated primarily by helper (CD4-positive) T cells, which produce interleukins
    • The effector functions are carried out primarily by cytotoxic (CD8-positive) T cells, which kill virus-infected cells, tumor cells, andallograft
  106. helper T cells make:
    • – (1) interleukin-4 (IL-4) and IL-5, which help B cells produce antibodies
    • – (2) IL-2, which activates CD4 and CD8 cells
    • – (3) gamma interferon, which activates macrophages, the main mediators ofdelayed hypersensitivity against intracellular organisms such asMycobacterium tuberculosis.
  107. Helper T Lymphocytes functions
    • “Help” the antigen-driven maturation of B and T cells
    • Facilitate and magnify the interaction between APCs (antigenpresenting cells) and immunocompetent lymphocytes
  108. Binding antigen to T cell receptors allows:
    • – Direct killing of foreign or abnormal cells
    • – Assistance or activation of other cells
  109. T regulatory cells (Treg) regulate the immune response to avoid
    attacking “self”
  110. B cells perform important functions:
    • (1) They differentiate into plasma cells and produce antibodies
    • (2) they can present antigen to helper T cells
    • (3) responsible for humoral immunity which involves "free"circulating antibodies secreted by cells.
  111. Epitopes are 
    Antibody connection site on bacterial cell (antigenic determinants on antigen)
  112. Immunoglobins, or antibodies, are serum glycoproteinsproduced by plasma cells in response
    to a challenge by animmunogenic antigen.
  113. Humans have five classes of immunoglobulins that function in
    antibody-antigen binding.
  114. Most predominant immunoglobulin is
    • IgG
    • The domain near upper end of the ‘Y’ shape are hyper-variable
    • A given immunoglobulin generally binds to only a part, called theepitope of a large antigen
    • Binding often involves a conformational change in the IgG
  115. Antigen Binding
    • Amino acid sequences of the variable regions of the heavy andlight chains
    • Framework regions control antibody folding
    • Lock and key
    • Antibody valence
  116. Antibody valence
    • IgG, IgD, and IgE—2
    • IgA—4
    • IgM—theoretically 10, likely 
  117. Main antibody in the secondary response. Opsonizes bacteria, making them easier to phagocytose. Fixes complement, whihc enhances bacterial killing. Neutralized bacterial toxins and viruses. Crosses the placenta 
    Name the following Immunoglobulin
  118. Secretory prevents attachment of bacteria and viruses to mucous membranes. Does not fix complement 
    Name the following Immunoglobulin
  119. Produced in the primary response to an antigen. Fixes complement. Does not cross the placenta. Antigen receptor on the surface of B cells 
    Name the following Immunoglobulin
  120. Found on the surfaces of B cells where it acts as a receptor for antigen
    Name the following Immunoglobulin
  121. Mediates immediate hypersensitivity by causing release of mediators from mast cells and basophils upon exposure to . antigen (allergen). Defends against worm infection. Does not fix complement. Main host defense against helminthic infections
    Name the following Immunoglobulin
  122. Antibody direct function 
    • – Neutralization
    • – Agglutination
    • – Precipitation
  123. Antibody indirect function 
    – Opsonization
  124. mechanisms of pathogenesis
    Portal of Entry 
    • Mucous membranes
    • Respiratory Tract
    • Gastrointestinal Tract 
    • Genitourinary Tract 
    • Skin 
    • Parenteral Route
  125. mechanisms of pathogenesis
    Penetration or Evasion of Host Defenses
    • Capsule 
    • Cell wall components
    • Enzymes 
    • Antigenic Variation 
    • Invasins 
    • Intracellular growth 
  126. Damage to Host Cells 
    • Siderophores 
    • Direct damage 
    • Toxins = Exotoxins, Endotoxins
    • Lysogenic conversion 
    • Cytopathic effects
  127. Portals of exit 
    Generally the same as the portals of entry for a given microbe
  128. Infection
    Pathogens present: may infect others
  129. Infection
    Attaches to host cells via adhesion molecules and receptors: cell injury, alteration in function or death 
  130. Infection 
    Uses host nutrients/enviroment :tissue damage, disease symptoms
  131. Infection 
    Migration through tissue, circulatory, or lymph systems: disease
  132. Normal Colonizationin Digestive Tract
    • Produce enzymes that help digestion
    • Produce antibacterial factors
    • Produce metabolites (Vitamin K & B)
    • Maintained by system integrity/immune systems
  133. Factors influencing disease development
    – Entry portal:
    spread is easy through blood and lymph systems
  134. Mechanism of action:
    how does it damage cells?
  135. Infectivity:
    ability to enter and replicate
  136. Pathogenicity:
    ability to produce disease
  137. Virulence
    speed of replication
  138. Toxigenicity
    production of toxins
  139. Viruses are intracellular parasites do not have
    • organelles necessary for reproduction
    • – Replicate by “taking over” the metabolic systems of host cell
    • – May kill cell, coexist with cell, be killed by immune system
  140. Vaccination is based on strategy of
    ‘training the immune system’ to recognize antigens from pathogenic agents
  141. Vaccine antigen is
    inactivated and/or neutralized, but ‘shape’is retained to provide unique epitope
  142. Immune system forms ‘memory’ to
    vaccine antigen
  143. Vaccine for Diphtheria disease is 
    Purified Diptheria Toxoid 
  144. Vaccine for meningococcal 
    Purified polysaccharide from Neisseria meningitidis
  145. Vaccine for Pertussis 
    Killed whole or acellular fragments of Bordella pertussis 
  146. Vaccine for Pneumococcal pneumonia 
    Purified polysaccharide from 7 strains of streptococcus pneumoniae 
  147. Vaccine for Tetanus 
    Purified Tetanus Toxoid 
  148. Vaccine for Haemophilus influenzae type b meningitis
    Polysaccharide from Haemophilus influenza type b conjugated with protein
  149. Influenza 
    Type of Vaccine Virus
    Injected vaccine, inactivated virus (nasally administered: attenuated virus)
  150. MMR 
    Type of Vaccine Virus
    Attenuated virus
  151. Chicken Pox 
    Type of Vaccine Virus
    Attenuated virus
  152. Poliomyelitis
    Type of Vaccine Virus
    Killed Virus
  153. Different cells and proteins involved in inflammation
    • Mast cells, Granular cells, Macrophages and their critical role
    • Complement: 3 pathways
  154. First line of defense
    Physical and biochemical
  155. Second line of defense:
    • Inflammation•
    • What processes constitute ‘inflammation’
  156. T cells and role in adaptive immunity
    cell mediated immune response)
  157. B cells and role in adaptive immunity
    Antibodies• Antibody-mediated immune response (humoral immunity)
  158. Epidemiology 
    is the study (or the science of the study) of the patterns,causes, and effects of health and disease conditions in definedpopulations
  159. Attenuated micro
    • microbes are changed in a host and extrated for use as a vaccine 
    • Ex. Human Virus to Chimp Extrated for use as vaccine 
  160. Allergy/Hypersensitivity
    Exaggerated immune response against environmental antigens
  161. Autoimmunity
    Mis-directed response against the host’s own cells (autoimmunity)
  162. Alloimmunity
    • Immune response directed against beneficial foreign tissue
    • – Transplants and transfusions
  163. Immune Deficiency
    Insufficient immune response to protect the host
  164. Altered immunologic response to an antigen that results indamage or disease to the host.
    Is what type of sensativity
  165. Allergy response:
    deleterious effects of hypersensitivity toenvironmental antigens
  166. Source of the antigen
    • Allergy
    • autoimmune
    • alloimmune
  167. A protective response to antigens expressed by disease causing agents is known as
    Immune Response
  168. Factors associated with hypersensitivity
    • – Genetics
    • – Prior Infections
    • – Environmental Factors
  169. An individual is sensitized when an adequate amount of
    antibodies or T cells are available to cause a noticeable reaction on re-exposureto the antigen.
  170. Type 1 reactions are mediated by
    antigen-specific IgE and the products of tissue mast cells.
  171. Most common allergies are type I reactions such as 
    Provoked by environmental allergens
  172. Acting through H1 receptors, histamine does the following
    • • Contracts bronchial smooth muscles
    • • Increases vascular permeability
    • • Causes edema
    • • Causes vasodilation
  173. Type II Hypersensitivity
    Tissue specific
    Specific cell or tissue (tissue-specific antigens) is the target of animmune response
  174. Five mechanisms
    • – Cell is destroyed by antibodies and complement
    • – Cell destruction through phagocytosis
    • – Soluble antigen may enter the circulation and deposit on tissues
    • – Antibody-dependent cell-mediated cytotoxicity
    • – Causes target cell malfunction
  175. Type III Hypersensitivity
    • Immune complex mediated
    • Antigen-antibody complexes formed in the circulation and laterdeposited in vessel walls or extravascular tissues
    • Not organ specific
    • Immune complex clearance
  176. Major difference between Type II and Type III is that
    Type II antibodybinds to antigen on cell surface, whereas Type III, antibody binds tosoluble antigen released into blood or body fluids and complex isdeposited in tissues
  177. Immune complex clearance
    • – Large—macrophages
    • – Small—renal clearance
    • – Intermediate—deposit in tissues
  178. Examples of Immune Complex–Mediated Diseases: Type III
    • • Systemic lupus erythematosus
    • • Vasculitis• Post-streptococcal glomerulonephritis
    • • Acute glomerulonephritis
    • • Reactive arthritis
  179. Antigenic Targets of Hypersensitivity Reactions
    – Self Antigens, with damage to host tissues
  180. Antigenic Targets of Hypersensitivity Reactions
    – Against foreign tissue Antigens
  181. Mechanism for desensitization:
    • Production of large amounts of blocking antibodies
    • Reduced capacity to ‘recognize’ antigen
  182. Production of large amounts of blocking antibodies
    • Blocking antibody competes in the tissues or in the circulation forbinding with antigenic determinants on the allergan so that theallergen is neutralized and unable to bind with IgE on mast cells.
    • Blocking antibody binds with IgE instead of the allergan
  183. Autoimmunity
    Breakdown of ‘tolerance’
    Body recognizes self-antigens as foreign
  184. Autoimmunity 
    Sequestered antigen
    • Self-antigens not normally seen by the immune system
    • Can occur in ‘privileged’ sites (anterior chamber of eye; brain)
  185. Autoimmunity 
    Infectious disease
    Molecular mimicry (pathogen mimics a self-antigen and then self-antigengets recognized as foreign)
  186. Autoimmuity 
    Haptens (new antigens or neoantigens) become immunogenic when theybind to host, or self proteins – autoimmune thyroiditis
  187. Antibodies are usually of the
    IgM class
  188. Blood Type A is incompatible with blood type
    B & AB
  189. Blood Type B is incompatible with blood type
    A & AB
  190. Blood Type AB is incompatible with blood type
    Universal Recipient Incompatiblee with none
  191. Blood Type O is incompatible with blood type
    A & AB Universal Donor 
  192. epi (upon)+demos (people)+logy (study of)
    “Epidemiology is the study of how disease is distributed in populations and thefactors that influence or determine this distribution.”
  193. One exposure, common vehicle
    • All cases develop by exposure to the same agent (germ, food, etc)
    • Exposure occurs only once
    • Outbreak is generally explosive• Sudden and rapid increase in number of cases
  194. Examples of Immune Complex–Mediated Diseases: Type III
    • • Systemic lupus erythematosus
    • • Vasculitis
    • • Post-streptococcal glomerulonephritis
    • • Acute glomerulonephritis
    • • Reactive arthritis
  195. Type IV hypersensitivity, in contrast to Types I-III, is mediatedby
    T lymphocytes and not antibody
  196. Most common allergies are type I hypersensitivities such as
    Pollens, molds, fungi, foods, animals, house dust, etc.
  197. Allergans that elicit Type IV Hypersensitivities
    Plant resins (poison ivy), metals, chemicals
  198. Graft Rejection
    – Chronic
    • • Months or years
    • • Inflammatory damage to endothelial cells of vessels due to a weakcell-mediated reaction against minor HLA antigens
  199. Graft Rejection
    – Acute
    • Cell-mediated response against unmatched HLA antigens
  200. Graft Rejection
    • • Immediate and rare
    • • Preexisting antibody to the antigens of the graft
  201. Immunodeficiency syndromes, whether congenital,spontaneously acquired, or iatrogenic (unknown cause), arecharacterized by
    unusual susceptibility to infection and arefrequently associated with autoimmune disease andlymphocyte related cancer. The types of infection often providethe first clue to the nature of the immunologic defect.
  202. Patients with defects in humoral immunity have recurrent or chronic
    sinopulmonary infection, meningitis, and bacteremia, most commonlycaused by pyogenic bacteria such as Haemophilus influenzae,Streptococcus pneumoniae, and Staphylococcus aureus.
  203. Abnormalities of T cell-mediated immunity predispose to disseminated
    virus infections, particularly with latent virusessuch as Herpes simplex, Varicella zoster, and cytomegalovirus
  204. Modes of Disease Transmission
    • (transmission that does not involve person-to-person)
    • – Common vehicle (example: door handle, public telephone)
    • • Single exposure
    • • Multiple exposures
    • • Continuous exposure
  205. Modes of Disease Transmission
    A carrier, usually an insect or other arthropod, that transmits the causative organisms ofdisease from infected to non-infected individuals
  206. Modes of Disease Transmission
    • Person-to-person contact
    • • Blood• Airborne• Water
  207. Endemic
    • is defined as the habitual presence of a disease within a givengeographic area
    • – Usual occurrence of given disease within such an area
  208. Epidemic
    Occurrence in a community or region of a group of illnesses of similar nature,clearly in excess of normal expectancy, and derived from a common source orfrom a propagated source
  209. Pandemic
    • – Worldwide epidemic
    • – H1N1 or swine flu was recently declared a pandemic
  210. Disease Outbreaks\
    • One exposure, common vehicle
    • – All cases develop by exposure to the same agent (germ, food, etc)
    • – Exposure occurs only once
    • – Outbreak is generally explosive
    • • Sudden and rapid increase in number of cases
  211. Cases rarely occur in persons who acquire the disease from aprimary case
    • Secondary disease transmission is infrequent
  212. – Single exposure, multiple exposures, or continuous exposure
    • Food outbreaks are usually single, but can be multiple if source remains undetected.
    • Continuous source is represented by level of exposure that is persistent
  213. Outbreak analysis
    • – Person: who is, or who are the case(s)?
    • – Place: where was the case infected?
    • – Time: when did infection occur?
Card Set
Microbiology Lecture Week 3
Lecture Week 3