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   Like other infectious agents,parasites also induces
    immune resistance in its host.

   Immunological protection against parasitic infection
    is much less efficient.
   Malaria      - Plasmodium vivax

   Amoebiasis   - Entamoeba histolytica

   Leishmaniasis - Leishmania
There are two main types types of immunity:
 Innate

 Acquired
   SKIN:
    Forms an important barrier of penetration.
    eg: W.bancrofti
   BODY SECRETIONS:
    Intestinal secretions wash away luminal parasites
    eg: Trichinella spiralis
   MACROPHAGES:
    Attack parasites and destroy them
   RED CELL STRUCTURE:
   HbS provide resistance to P.falciparum
   G-6PD deficient people provide resistance to
    P.falciparum
   Antibody response

   Cellular response
   Specific immune responses to parsites results in
    antibody production.
   Produced by plasma cells
   Mainly IgG and IgM
   Helminthic infection-IgE
   NEUTRALISATION :
   Antibody combines with surface molecule of
    parasite and neutaralise them.
   Block attachment to host cells
   Antibody binds to toxins and enzymes of parasites,
    thus protecting host.

   AGGLUTINATION:
   Agglutination of blood parasite by IgM antibody
   Prevents spread of parasite
   Eg trypanosoma cruzi
   OPSONISATION:
   Antibody can act as opsonin and enhances clearances
    by phagocytes
   eg.protozoa
   PHYSICAL CLEARANCE :
   Block orifices of certain worms and can cause
    starvation or curtail reproduction.
   ANTIBODY DEPENDENT CYTOTOXICITY:
   Complement mediated cell lysis
   Effector cells,macrophages,monocytes , neutrophils
    and eosinophils combine with Fc and complement
    receptors of antibody coated parasites.
   T-LYMPHOCYTES:
   CD 4+T cells act as helper cells in antibody
    production
   CD+8 cells are cytotoxic
   MACROPHAGES:
   Play dominant role in process of elimination of
    protozoa or worms
   GRANULOCYTES:
   Neutrophils and eosinophils play important role in
    elimination of protozoa and helminthes
THE PATHWAY OF SPECIFIC IMMUNE RESPONSE

              Step 1
              Pathogens eaten by Macrophage



                                      Step 2
                                      Displays portion of Pathogen
                                      on surface




                                                Step 3

Pathogens



               Helper-T cell recognizes
               Pathogen
Activates Cytotoxic                       Activates B- Cell

T- Cell




                                       Memory B-Cell
                       Memory T-Cell

                                             Antibodies
Kills Infected Cells
IMMUNE RESPONSE SUMMARY
                                                   Antigen
                                                                           Displays copy of antigen
                                                                           on surface of cell
                                                Macrophage



                                                Helper T - Cell
         Cellular                                                               Antibody Immunity
         Immunity
             Active Cytotoxic T-Cell                                             Active B - Cell



Kills Infected Cells           Memory T- Cell                     Plasma Cell                      Memory B-Cell



                                                                  Antibodies



                                                             Deactivates Antigens
   Complexity of parasitic structure.

   Complexity of parasitic life cycle

   Immune evasion

   Larger size of parasites

   Intracellular location of many protozoa
   Successful parasites have evolved
    strategies for survival & development
   INTRACELLULAR HABITAT:
   Parasites may live intracellularly. By replicating
    inside host cell parasites avoid immune response.
   Plasmodium lives inside Red Blood Cells (RBC’S)
    which have no nucleus, when infected not
    recognised by CTL’s & NK cells. Other stages of
    Plasmodium live inside liver cells.
   ANTIGENIC VARIATIONS:
    In Plasmodium, different stages of the life cycle
     express different antigens. We will describe evasion
     strategies of Plasmodium in more detail in the next
     lecture.
    Antigenic variation also occurs in the extracellular
     protozoan, Giardia lamblia.

    ANTI-IMMUNE MECHANISMS:
    Leishmania produce anti-oxidases to counter
     products of macrophage oxidative burst
   IMMUNOSUPPRESSION:
   manipulation of the immune response. High
    burdens of nematode infection often carried with
    no outward sign of infection.
   Growing evidence that parasite secreted products
    include anti-inflammatory agents which act to
    suppress the recruitment and activation of effector
    leukocytes.
   E.g. a hookworm protein which binds the ß
    integrin CR3 & inhibits neutrophil extravasation.
   MIGRATION:
   Hookworms, move about gut avoiding local
    inflammatory reactions.
   PRODUCTION OF ENZYMES:
   Filarial parasites secrete a number of anti-oxidant
    enzymes such as glutathione peroxidase &
    superoxide dismutase which most likely contribute
    to their observed resistance to antibody-dependent
    cellular cytotoxicity and oxidative stress.
Chronic suppurative otitis media-Tubotympanic type

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Chronic suppurative otitis media-Tubotympanic type

  • 1.
  • 2. Like other infectious agents,parasites also induces immune resistance in its host.  Immunological protection against parasitic infection is much less efficient.
  • 3. Malaria - Plasmodium vivax  Amoebiasis - Entamoeba histolytica  Leishmaniasis - Leishmania
  • 4. There are two main types types of immunity:  Innate  Acquired
  • 5. SKIN: Forms an important barrier of penetration. eg: W.bancrofti  BODY SECRETIONS: Intestinal secretions wash away luminal parasites eg: Trichinella spiralis  MACROPHAGES: Attack parasites and destroy them  RED CELL STRUCTURE:  HbS provide resistance to P.falciparum  G-6PD deficient people provide resistance to P.falciparum
  • 6. Antibody response  Cellular response
  • 7. Specific immune responses to parsites results in antibody production.  Produced by plasma cells  Mainly IgG and IgM  Helminthic infection-IgE
  • 8. NEUTRALISATION :  Antibody combines with surface molecule of parasite and neutaralise them.  Block attachment to host cells  Antibody binds to toxins and enzymes of parasites, thus protecting host.  AGGLUTINATION:  Agglutination of blood parasite by IgM antibody  Prevents spread of parasite  Eg trypanosoma cruzi
  • 9. OPSONISATION:  Antibody can act as opsonin and enhances clearances by phagocytes  eg.protozoa  PHYSICAL CLEARANCE :  Block orifices of certain worms and can cause starvation or curtail reproduction.  ANTIBODY DEPENDENT CYTOTOXICITY:  Complement mediated cell lysis  Effector cells,macrophages,monocytes , neutrophils and eosinophils combine with Fc and complement receptors of antibody coated parasites.
  • 10. T-LYMPHOCYTES:  CD 4+T cells act as helper cells in antibody production  CD+8 cells are cytotoxic  MACROPHAGES:  Play dominant role in process of elimination of protozoa or worms  GRANULOCYTES:  Neutrophils and eosinophils play important role in elimination of protozoa and helminthes
  • 11. THE PATHWAY OF SPECIFIC IMMUNE RESPONSE Step 1 Pathogens eaten by Macrophage Step 2 Displays portion of Pathogen on surface Step 3 Pathogens Helper-T cell recognizes Pathogen
  • 12. Activates Cytotoxic Activates B- Cell T- Cell Memory B-Cell Memory T-Cell Antibodies Kills Infected Cells
  • 13. IMMUNE RESPONSE SUMMARY Antigen Displays copy of antigen on surface of cell Macrophage Helper T - Cell Cellular Antibody Immunity Immunity Active Cytotoxic T-Cell Active B - Cell Kills Infected Cells Memory T- Cell Plasma Cell Memory B-Cell Antibodies Deactivates Antigens
  • 14. Complexity of parasitic structure.  Complexity of parasitic life cycle  Immune evasion  Larger size of parasites  Intracellular location of many protozoa
  • 15. Successful parasites have evolved strategies for survival & development
  • 16. INTRACELLULAR HABITAT:  Parasites may live intracellularly. By replicating inside host cell parasites avoid immune response.  Plasmodium lives inside Red Blood Cells (RBC’S) which have no nucleus, when infected not recognised by CTL’s & NK cells. Other stages of Plasmodium live inside liver cells.
  • 17. ANTIGENIC VARIATIONS:  In Plasmodium, different stages of the life cycle express different antigens. We will describe evasion strategies of Plasmodium in more detail in the next lecture.  Antigenic variation also occurs in the extracellular protozoan, Giardia lamblia.  ANTI-IMMUNE MECHANISMS:  Leishmania produce anti-oxidases to counter products of macrophage oxidative burst
  • 18. IMMUNOSUPPRESSION:  manipulation of the immune response. High burdens of nematode infection often carried with no outward sign of infection.  Growing evidence that parasite secreted products include anti-inflammatory agents which act to suppress the recruitment and activation of effector leukocytes.  E.g. a hookworm protein which binds the ß integrin CR3 & inhibits neutrophil extravasation.
  • 19. MIGRATION:  Hookworms, move about gut avoiding local inflammatory reactions.  PRODUCTION OF ENZYMES:  Filarial parasites secrete a number of anti-oxidant enzymes such as glutathione peroxidase & superoxide dismutase which most likely contribute to their observed resistance to antibody-dependent cellular cytotoxicity and oxidative stress.