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Immunity against Parasitic infection

Immunity against Parasitic infection. Prof. dr. Supargiyono DTM&H, PhD, SpParK. Department of Parasitology FM. UGM. Parasitic infection. Parasitic infection is caused by animal parasite : protozoa pathogenic: Rhizopoda Entamoeba histolytica, Entamoeba coli Ciliata: Balantidium coli

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Immunity against Parasitic infection

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  1. Immunity against Parasitic infection Prof. dr. Supargiyono DTM&H, PhD, SpParK. Department of Parasitology FM. UGM.

  2. Parasitic infection • Parasitic infection is caused by animal parasite: • protozoa pathogenic: • Rhizopoda • Entamoeba histolytica, • Entamoeba coli • Ciliata: Balantidium coli • Flagelata : • Trichononas vaginalis • Giardia lamblia • blood & tissue : • Plasmodium falciparum, • P. vivax, • P. malariae, • P. ovale , P. knowlessi • Toxoplasma gondii; • Trypanosoma (Sleeping sickness), • Liesmania (skin lesion);etc.

  3. Helminthes : • Nematodes (round worm): • intestinal : Ascaris lumbricoides, Oxyuris vermicularis, Trichuris trichiura, Ancylostoma duodenale & Necator americanus (Hook worm); Soil Transmitted Helmithes (STH) • blood & tissue : Filarial worms : • Lymphatic: Wuchereria bancrofti, Brugia malayi, Brugia timori • Non-Lymphatic: Loa-loa, Onchocerca sp. • Cestodes (tape worm): Taenia saginata, T. solium, Diphylobothrium latum, Hymenolepis nana,E. granulosus, etc. • Trematodes (fluke): • Liver : Fasciola hepatica, • Intestinal : F. buski (intestine), • Lung : Paragonimus westermani, • Blood & Lymph : Schistosoma japonicum, S. mansoni, S. hematobium, etc. • Arthrophode (insect) : • ectoparasite (tick, mites, louse, etc)

  4. The prevalence : • More then 30% world population suffer parasitic infection • More in developing countries • Most parasites : • Go through complex life cycle • part of which in human and other vertebrate host • The other part in intermediate invertebrate host (mosquito, fish, flies, etc) Fasciolopsiasis

  5. Fundamental feature of parasitic infection • Most parasite produce chronic infection • Reasons : • in endemic area parasite persisted in favorable environment  available reservoir  produce repeated infection • weak natural immunity • infective stage are resistance to unfavorable environment • parasite are able to evade specific immune responses • many antiparasite antibodies are not-effective & toxic the parasite persist for long periode of time in the human body chronic immunologic reaction tissue damage/injury: Renal failure (malaria), elephantiasis (Filaria), Ascites (Schistosoma) , loefler syndrome (ascaris)), etc)

  6. Immunity against parasitic infections • Immunity to parasites : • Innate/Natural resistances  general • Acquired resistances  specific (antibody) • Most parasites (Protozoa & helminth) enter the body (GI tract, blood stream/tissue) passing Natural resistance (barrier) of the body • well adapted to resisting natural host defence (cyst of intestinal protozoa, worm eggs, hookworm larvae etc) • able to evade lysis by complement • able to survive inside phagocytic cells • integument of helminth resistant to cytosidal of neutrophylls and macrophage survive/multiplicates

  7. Specific immune responses to parasites • Parasites : Varies greatly : structure & molecular constituent Histamin, Proteases, Etc. variety of immune responses also different from bacteria & viruses

  8. Major pattern of specific Immune Responses to parasites • Production of specific IgE & Eosinophilia in helminthic infection Stimulation of Th2(CD4+TCell): • release IL4 (interleukin 4)  elevation of serum Ig E • release IL5 (interleukin 5)  eosinophilia IgE-dependent cytotoxicity by eosinophils is efective in killing some helmiths • Major basic protein of eosinophil granules are toxic for helminths Stimulation of Th1 (CD4+TCell)  IFNg  activation of M@  secretes NO & TNF (kill the parasites: malaria) Eosinophil MJP

  9. Major pattern of specific Immune Responses to parasites (cont) • Some parasites & their product induce granulomatous responses fibrosis • Schistosomamansoniegs in liver induce fibrosis  disrupt venous blood flow  portal hypertension  cyrhosis • Lymphatic filariasis, filarial worm in lymphatic vesel  chronic CMI  fibrosis  lymph-obstruction  severe chronic lymphedema  elephantiasis.

  10. Major pattern of specific Immune Responses to parasites (cont) • Protozoa that replicate inside cells (intracellular parasites) stimulate specific CTLs (cytotoxic T lymphocytes) • Extracellular parasite antigen stimulate antibody responses (humoral immune responses) Antigen-Antibody reaction complex  deposition tissue dammage (glomerulonefritis, renal failure, etc) Attached are pathology & imunology of some parasitic diseases

  11. Presentation of parasite antigen

  12. Immune responsis against intracellular parasites

  13. Oxyuris vermicularis Trichuris trichiura Loefler syndrome GI irritation : diarhea, naucea, vomitus, abdmnl discomfort Immunologis : elevation of IgE Eosinophillia, urticaria

  14. The hook worm Skin : alergic reaction Serum : IgE & Eosinophylia

  15. Trichinella spiralis

  16. Taenia saginata Cystecercuc bovis

  17. Eosinophills, IgE

  18. Immune Response to Filaria parasite Following infections high levels of anti-parasite IgE and IgG4 are produced which is generally accompanied by eosinophilia. This is due to the preferential stimulation of T-cells which produce IL-4 and IL-5(Th-2 type). (In asymptomatic microfilaremic patien) Elephantiasis may result from killing of late stage larval antigens by IgE mediated mechanisms or by a passive reaction of naturally dying adult worms, evoking inflammatory reactions. The patients withtropical pulmonary eosinophilia (TPE)elicit a very high IgE response which is predominantly developed against microfilaria. In TPE mf are not found since the immunological hyper-responsiveness removes this stage of the parasite from circulation.

  19. Entamoeba hystolitica

  20. Malaria P. falciparum  malignant Tertian malaria P. vivax  benign tertian malaria P. malariae - Quartant malaria P. ovale  malaria ovale ring Clinical manifestation : due to erythrocytic stage Infected RBC adhered to endothelial cell in some organ (cytoadherent) Normal RBC adhered to infected RBC  rosetting  Sequestration Intermitten fever: due to ruspture of RBC released toxic product Spleen : important organ of the immune system splenomegaly & macrophage hyperplasia : hallmark of malaria Splenic macrophages full of parasitic pigments.

  21. References: • Abul K. Abbas, Andrew H. L., Jordan S.P. 1994. Cellular and Molecular Immunology. Second edition. W.B. SOUNDERS Co. • Jeffrey H.C. and Leach R.M., 1975. Atlas of Medical Helminthology and Protozoology, Second edition. Churchil Livingstone, London.

  22. Good Luck

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