Immunity to Veterinary parasitic infections power point presentation

IMMUNOLOGY

1. JIMMA UNIVERSITY COLLEGE OF AGRICULTURAL AND VETERINARY MEDICINE SCHOOL OF VETERINARY MEDICINE Immunology group assignment PREP. BY Besheda wedajo bikila (DVM) TITLE: IMMUNITY to PARSITIC INFECTION jimma , 2024

2. Introduction The term ‘ parasite ’ is used to denote an organism that is dependent on another organism i.e. the host for its survival. I mmunity refers to the resistance of the host to invasive pathogens and their toxins. As the parasite attacks the host, the two come into a close dynamic interaction. While the parasite tries to establish itself in/or the body of the host, the host mounts a series of immune defensive actions against the parasite.

3. NOTE Parasites tend to be more specific when it comes to the kind of host they will infect. This host specificity is governed by the parasite’s preference for age, sex and gender of the host and also by the broad molecular patterns involved in host-cell recognition. Parasite Associated Molecular Patterns (PAMPs) are distinct evolutionarily conserved structures present on the parasite’s surface. These recognize and bind to Pattern Recognition Receptors (PRRs), a family of Toll-like receptors (TLRs) on host macrophages and dendritic cells.

4. Cont.. Specificity differences can also result from subtle variations in genetic determinants of the host It has been found that individuals heterozygous for the Sickle cell i.e. possessing a defective form of haemoglobin ( HbS ) are more resistant to Plasmodium. Similarly, absence of duffy blood group antigens ( Fy ) makes an individual resistant to malaria, as is seen in many parts of Africa.

5. Cont.. Another parasite-derived factor is that the presence of one parasite may affect the growth of another in the same host. For example, the presence of adult worms in the host body often delays the establishment/development of larval stages of the same species. This phenomenon of ‘concomitant immunity’ is seen in case of infection with S.mansoni , Echinococcus granulosus .

6. 1.Innate Immune Response N onspecific immunity acts as the first line of the defensive mechanism Anatomical and Structural barriers defense of the host’s body These include: Epithelial surface of skin (except at places of cut or abrasion) Body secretions: tears, saliva, sweat and secretions of the gastrointestinal and vaginal tracts which flush out invading parasites Movement due to cilia and gut peristalsis Mucous membranes lining the respiratory, gastrointestinal tract Cough reflexes

7. 2. Specific immunity (Adaptive) This is formed of two major components: Humoral immune response : Carried out by B-lymphocytes which differentiate into antibody producing cells. Works in the interaction of B cells with antigen and their subsequent proliferation and differentiation into antibody-secreting plasma cells Antibody functions as the effector of the humoral response by binding to antigen and neutralizing it or facilitating its elimination

8. 2. Cellular immune response : Carried out by T-lymphocyte populations which have been found to be constituted by 3 main subpopulations : First subpopulation is constituted by the helper T-lymphocytes which assist the triggering of humoral and cellular immune responses. Second subpopulation is constituted by the cytotoxic T-lymphocytes which are able to destroy cells expressing non self or altered cell antigens. Third subpopulation of suppressor T-cells which are able to turn down unnecessary responses, such as those directed against self or against one antigen which has already been eliminated.

9. Cont.. Other cells such as the monocytes , macrophages and specialized macrophage derived cells found in many tissues. They play important roles by modifying and presenting antigens to lymphocytes and releasing soluble factors (interleukins) which regulate the activity of lymphocytes. The regulatory populations (helper and suppressor) of T-lymphocytes also release a variety of interleukins which participate in activation and suppression circuits

10. Types of the most important antibodies: IgM : Large-sized molecule. – Is more potent than IgG . – Increases in early and acute infections IgG : - Small-sized molecule (only one that can pass placenta). Is the largest amount in serum. Increases in late and chronic infections.

11. Cont.. IgA : Presents in secretions of gastrointestinal and urinary tracts. Resistant to proteolytic digestion. IgE ( reagenic antibody): Responsible for immediate hypersensitivity reaction Binds tightly to mast cells and basophils . When coated mast cells interact with specific antigen, they release potent mediators, including histamine and chemotactic factors attracting eosinophils . The released mediators may affect parasite directly or the accumulated eosinophils may be cytotoxic to parasite.

12. Types of parasitic antigens: Somatic: Somatic antigens are derived from the body (soma) of the parasite itself. either pieces of injured parasites or cuticular antigens from the tegument of the parasites. play an important role in the host-parasite interaction and can elicit immune responses in the host organism. 2. Excretory or metabolic may be: Metabolic products of the parasites. Enzymes. Secretory products. Cysteine proteases

13. Evasion and suppression of immune mechanisms Site of parasite: Intracellular parasites: RBCs: Malaria infected RBCs have a variety of plasmodial antigens on the erythrocytes surface, but the covering of RBCs by MHC (major histocompatibility ) antigens prevents recognition of parasitized cells by T- lymphocytes. Macrophages: Pathogenic protozoa proliferating within macrophages are covered with a membrane, called phagosomal membrane, which when get in contact with lysosomes , they fuse together leading to release of lysosomal enzymes toxic to parasite. These parasites can avoid lethal effects of this fusion by various mechanisms:

14. Cont.. Trypanosoma cruzi —> lyses the phagosomal membrane and once released into cytoplasm, can replicate progressively. b) Toxoplasma —> prevents fusion of phagosomal membrane with lysosome due to modification in phagosomal membrane. c) Leishmania —> does not affect fusion process but it resists damage by generation of enzymes and metabolic products which neutralize lysosome enzymes. 2. Parasite surrounds itself by fibrous tissue : as hydatid cyst and Coenurus cerebralis .

15. B. Modification of parasite antigenicity : 1. Antigenic variations : African trypanosomes are present in parasitaemic waves due to the recurrent formation of variable surface glycoproteins which are changeable from time to time. This explains periodicity of fever in African trypanosomiasis . 2. Shedding and renewal of surface antigens : This process is common among protozoal and helminthic pathogens e.g. in Schistosoma , viable schistosomulae shed the majority of cercarial membrane soon after skin penetration including their surface antigens

16. Cont.. 3. Antigenic masking (Molecular mimicry): Schistosomes mask themselves by taking host antigens on their surfaces e.g. MHC antigens —> these are called eclipsed antigens. - Also, schistosomes are able to synthesize antigens which cross react with host molecules, thus sharing the same host antigens —> this phenomena called molecular mimicry.

17. C. Modification and suppression of host immune response : Antibody cleavage : Schistosoma mansoni is able to produce proteolytic enzymes which can cleave antibody at FC region. Consumption of complement: Some parasites as Echinococcus granulosus produces antibodies which consume serum complement —> abolishing its effect. Immune suppression : Some parasites induce specific immune suppression in the host e.g. a) Leishmania donovani : suppresses T-cell responses, although there is large amount of specific antibodies produced. b) African trypanosomes: suppress or diminish both humoral and cell mediated responses, although IgM is constantly raised.

18. Con.. 4 . Modification of leucocytic function : Schistosoma mansoni adults modify leucocytic function by: Secretion of SDIF ( Schistosoma derived inhibitory factor) and formation of immune complexes which inhibit lymphocyte transformation and mast cell degranulation .

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