chronic suppurative otitis media-tubotympanic type
DESCRIPTION
CSOM TTDTRANSCRIPT
IMMUNITY IN PARASITIC INFECTION
Like other infectious agents,parasites also induces immune resistance in its host.
Immunological protection against parasitic infection is much less efficient.
EXAMPLES OF PARASITIC INFECTION
Malaria - Plasmodium vivax
Amoebiasis - Entamoeba histolytica
Leishmaniasis - Leishmania
There are two main types types of immunity:
Innate Acquired
IMMUNITY IN PARASITIC INFECTION
INNATE IMMUNITY 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
ACQUIRED IMMUNITY
Antibody response
Cellular response
ANTIBODY RESPONSE
Specific immune responses to parsites results in antibody production.
Produced by plasma cells Mainly IgG and IgM Helminthic infection-IgE
HUMORAL DEFENCE MECHANISM
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.
CELLULAR RESPONSE
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
Pathogens
Pathogens eaten by Macrophage
Displays portion of Pathogen on surface
Helper-T cell recognizes Pathogen
Step 1
Step 2
Step 3
Activates B- CellActivates Cytotoxic
T- Cell
Memory B-CellMemory T-Cell
Kills Infected Cells
Antibodies
IMMUNE RESPONSE SUMMARY
Displays copy of antigen on surface of cell
Cellular Immunity
Antibody Immunity
IMMUNE RESPONSE TO PARASITIC INFECTION IS COMPLEX
Complexity of parasitic structure.
Complexity of parasitic life cycle
Immune evasion
Larger size of parasites
Intracellular location of many protozoa
IMMUNE EVASION MECHANISMS OF PARASITES
Successful parasites have evolved strategies for survival & development
ESCAPE MECHANISMS: 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.
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