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.

THANK YOU