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Immunity .pptx pathology for mbbs students
- 1. IMMUNITY BY : DRSUSHMA CHOURASIA
- 2. DEFINITION • Resistance acquiredby a host towards injury caused by microorganisms and their products. • Protection against the infectious diseases which is one of the consequences of the immune response and it is entirely concerned with the reaction of the body against any foreign antigen.
- 3. TYPES OF IMMUNITY •Innate immunity • a. Nonspecific Species • b. Specific Racial Individual • Adaptive Immunity: • a. Active : Natural Artificial • b. Passive: Natural Artificial
- 6. INNATE IMMUNITY • Resistanceto infection which an individual possesses by virtue of his genetic and constitutional makeup Not affected by prior contact with microorganisms or immunization. • a. Non specific : Indicate a degree of resistance to infections generally. • b. Specific: Resistance to a particular pathogen.
- 9. INNATE IMMUNITY • 1.Species immunity: Resistance to pathogen, shown by all members of a particular species. E.g. anthracis infects human beings but not chickens. • 2. Racial Immunity: Within a species, different races may show difference in susceptibility to infections. E.g. Genetic resistance Plasmodium falciparum malaria resistance in Africa
- 10. • 3. Individual– immunity Resistance to infection varies with different individuals of same race and species. • E.g.. Homozygous twins exhibit similar resistance susceptibility to leprosy and Tuberculosis such correction is not seen in heterozygous twins.
- 11. FACTORS INFLUENCING INNATEIMMUNITY • 1. Age : In foetus immune system is immature, in old age there is gradual waning of immune system E.g. Polio infection , and Chickenpox highly severe in adult than children. • 2. Hormonal : Enhance suseptability to infection such as E.g. Diabetes mellitus • Hypothyroidism in adults • Adrenal dysfunction • 3. Nutrition E.g. Malnutrition predisposes to bacterial infection. • Both humoral and cell mediated immune responses are reduced in malnutrition.
- 12. MECHANISM OF INNATEIMMUNITY • 1. Epithelial surface: • a. Skin: • It acts as a machanical barrier to microorganisms and provide bactericidal secretions. • • Microflora of skin and mucous membrane surface help to prevent colonisation by pathogens. • • Alteration of normal resident flora may lead to invasion by extraneous microbes and thus causing serious disease. • • e.g Clostridial enterocoloitis following oral antibiotics
- 13. • b. Respiratorytract: • Inhaled particals are arrested in the nasal passage on the moist mucous membrane surface. • Mucous membrane acts as a trapping mechanism hair like cilia propels the particals towards pharynx where its swallowed or coughed out. • Cough reflex acts as a defence mechanism
- 14. • C. Intestinaltract: • Mouth possesses saliva which has a inhibitory effect on many microorganisms some bacteria are destroyed by acidic pH of gastric juices. • Normal bacterial flora of intestine exerts a protective colonisation of pathogenic bacteria. • d. conjunctiva: • Tears ( contain lysosyme which has anti bacterial property) helps in flusing away bacteria and other dust particals. e. Genitourinary tract • Flusing action of urine eliminates bacteria from ureter.
- 15. 2. ANTIBACTERIAL SUBSTANCE: •Nonspecific antibacterial substance present in the blood and tissue. • Substance like properiden, complement, lysosyme, betalysin, basic polypeptide and interferon which have antiviral activity. • Complement system plays an important role in destruction of pathogenic microorganisms that invade blood and tissue.
- 16. 3. CELLULAR FACTOR: •When infection cross the barrier of epithelial suface, tissue factor come into play for defence. • Exudate inflammatory reaction occurs by accumulation of phagocytes at the site of infection and deposition of fibrin which entangles the organisms to act as a barrier to spread of infection. • Phagocytic cells ingest these organisms and destroy them.
- 17. PHAGOCYTIC CELLS ARE •classified as: • i) Microphages e.g. polymorphomuclera leucocytes ( neutrophils) • ii) Macrophages e.g mononuclear phagocytic cells
- 18. PHAGOCYTIC ACTION • dividedinto 4 stages: • • i) Chemotaxis: Phagocytes reach the site of infection attracted by chemotactic substances. • ii) Attachment: Infective agent gets attached to phagocytic membrane. • iii) Ingestion: Phagoctes engulf the infective material into vacule Membrane of phagosome fuses with lysosomes to form a phagolysosome. • iv) Intracellular killing: Most bacteria are destroyed by phagolysosomes by hydrocytic enzymes of lysosomes Natural killer cells play a important role in non specific defence against viral infections and tumour.
- 19. INFLAMMATION • 4.Inflammation occuras a result of tissue injury or irritation, initiated by entry of pathogens or other irritants. It’s a nonspecific defence mechanism. • Inflammtion leads to vasodilatation, increased vascular permeability and cellular infiltration. Microorganisms are phagocytosed and destroyed due to increased vascular permeability, which helps to dilute the toxic products present. Fibrin barrier is laid to wall off site of infection.
- 20. • Fever: • Riseof temperature following infection is a natural defence mechanism. • It destroyes the infecting organisms. Fever also stimulates the production of interferon which helps in recovery from viral infection.
- 21. ACUTE PHASE PROTEIN •6. Following infection or injury, there is a sudden increase in plasma concentration of certain proteins, called acute phase proteins. • This include c-reactive protein, mannose binding protein etc CRP and acute phase protein activate alternative pathway of complement. • This is caused to prevent tissue injury and promote repair of inflammtion lesions.
- 23. ADAPTIVE IMMUNITY • Thisis inducible and develops slowly than the innate response. • This is specific kind of immunity that has memory, therefore providing long term protection. • This occurs with contact of foreign particle. Adaptive immunity is often sub- divided into two major types depending on how the immunity was introduced: • I. Naturally acquired immunity occurs through contact with a disease causing agent, when the contact was not deliberate. • II. Artificially acquired immunity develops only through deliberate actions such as vaccination.
- 24. MECHANISM • Active immunityresponse stimulates both humoral and cell mediated immunity. • i) Humoral immunity: It’s a antibody mediated immunity It depends on the synthesis of antibodies by plasma cells, the cells produce specific circulating antibody which combine specifically with the antigens and modify their activity.
- 25. • Modified activityis done by lysis of antigen molecules with their toxin may be neutralised or in the form of removal of antigen by phagocytosis. • ii) Cell mediated immunity: Depends on T- lymohocytes Cell mediated immunity by sensitised T lymphocytes helps in resistance to chronic bacterial infections in chronic infection, organisms can multiply and survive in phagolysosomes and In viral infections..
- 27. TYPES OF ADAPTIVEIMMUNITY • Active immunity : • a. Naturally acquired active immunity occurs when the person is exposed to a live pathogen, develops the disease, and becomes immune as a result of the primary immune response. • b. Artificially acquired active immunity can be induced by a vaccine, a substance that contains the antigen. A vaccine stimulates a primary response against the antigen without causing symptoms of the disease.
- 28. • Vaccine : •Live vaccine: BCG for tuberculosis, Sabin vaccine for poliomylitis Killed vaccine: Hepatitis B vaccine • non-neural vaccine for rabies Bacterial product: Tetanus toxoid vaccine, Deptheria toxoid for deptheria
- 29. PASSIVE IMMUNITY • A.Artificially acquired passive immunity is a short-term immunization by the injection of antibodies, such as gamma globulin, that are not produced by the recipient's cells. • Naturally acquired passive immunity occurs during pregnancy, in which certain antibodies are passed from the maternal into the fetal bloodstream
- 30. ACTIVE IMMUNITY • Inducedby infection • Long lasting and effective protection • Effective only after lag period • Exposure leads to immediate maximal response • Immunological memory present • Negative phase may occur • Not applicable to immunodeficient person
- 31. • Used forprophylaxis to increase body resistance e.g BCG vaccine Passive immunity • Conferred by administration of ready made antibodies. • Short lived and less effective • Effective immediately • Lag time between exposure and maximal response • No immunological memory • No negative phase • Applicable to immunodeficient person • Used for treatment of acute infection
- 32. ANTIGEN • An antigenis a molecule that induces an immune response in the body. • Origin of antigen • Exogenous antigens • Antigens that have entered the body from the outside. E.g. By inhalation, ingestion, or injection. • Endogenous antigens - Antigens that have been generated within previously normal cells as a result of normal cell metabolism, or because of viral or intracellular bacterial infection.
- 33. AN AUTOANTIGEN • isusually a normal protein or complex of proteins (and sometimes DNA or RNA) that is recognized by the immune system of patients suffering from a specific autoimmune disease. • These antigens under normal conditions, should not be the target of the immune system, but, due to mainly genetic and environmental factors, the normal immunological tolerance for such an antigen has been lost in these patients.
- 34. IMMUNOGEN • It isa substance or a mixture of substances that is able to provoke an immune response if injected to the body. • An immunogen is able to initiate an innate immune response first, later leading to the activation of the adaptive immune response, whereas an antigen is able to bind the highly variable immunoreceptor products (b-cell receptor or t-cell receptor) once these have been produced.