In spite of immune surveillance certain protozoans often enter the blood stream, become resistant to immune effector mechanisms. Some of the remarkably effective ways developed by protozoans to resist specific immunity are as follows:
1. Antigenic Masking:
Antigenic masking is the ability of a parasite to escape immune detection by covering itself with host antigens. Some protozoans become non immunogenic/ non antigenic by masking themselves with host antigens eg. Trypanosoma theileri in cattle, Trypanosoma lewisi in rat.
2. Blocking of Serum Factors:
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Some parasites acquire a coating of antigen- antibody complexes or noncytotoxic antibodies that sterically blocks the binding of specific antibody or lymphocytes to the parasite surface antigens.
3. Intracellular Location:
The anatomic sequestration (intracellular habitat) of some protozoan parasites protects them from the direct effects of the host’s immune response. Their intra cellular habitat conceals the parasite antigens and delays detection by the immune system. This is commonly observed with Plasmodium and T. gondi
4. Antigenic Variation:
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Some protozoan parasites change their surface antigens during the course of an infection. Parasites carrying the new antigens escape the immune response to the original antigens.
5. Antigen sheding:
Some protozoans shed their antigen coats either spontaneously or after binding with specific antibodies eg. E. histolytica.
6. Hypo immunogenic:
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Some protozoa become hypo immunogenic at certain stages of their life for example cyst stage of T.gondi will not stimulate host response.
7. Immunosuppression:
Parasitic protozoan infections generally produce some degree of host immunosuppression. This reduced immune response may delay detection of antigenic variants. It may also reduce the ability of the immune system to inhibit the growth of and/or to kill the parasites.
Sometimes immune suppression is caused directly by parasite products and sometimes involves antigenic mimicry, which often appears in association with parasitic diseases (abnormalities in cytokine production, deficient T cell activation) eg. Trypanosoma, Leishmania, Toxoplasma, Entamoeba.