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Immunity

Immunity powerpoint for Second MBBS Undergraduate students

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Immunity

  1. 1. IMMUNITY Dr. SOMESHWARANRAJAMANI,MBBS, MD., AssistantProfessor & ClinicalMicrobiologist, Karpagam Faculty of Medical Sciences and Research, Othakalmandapam, Coimbatore-641032
  2. 2. OBJECTIVES • To define immunity and to explain the types of immunity with examples. • To elucidate on innate immunity and explain in detail about adaptive immunity • To know the differences between innate and adaptive immunity • To summarize the methods of measuring immunity
  3. 3. Introduction • Host immune system Vs Foreign antigen. • One of the consequence of Immune response is protection against infectious diseases. • State of protection can be less specific or more specific depending on various factors. Immunity is the resistance exhibited by the self (host) towards the injury caused by microorganisms and their products.
  4. 4. Types of Immunity • Immunity against infectious disease is 2 types: 1. Innate or Native immunity 2. Adaptive or Acquired immunity
  5. 5. Immunity against infectious diseases Innate or Native immunity a. Non-specific b. Specific i. Species immunity i. Species immunity ii. Racial immunity ii. Racial immunity iii. Individual immunity iii. Individual immunity Adaptive or Artificial immunity a. Active immunity b. Passive immunity i. Natural i. Natural ii. Artificial ii. Artificial
  6. 6. Innate immunity • First line of defense against infections • Not affected by prior contact with infectious microorganisms or by immunisation. • Specific (resistance to particular pathogen) • Non-specific (general degree of resistance to infections) Innate immunity is the resistance to infections that an individual possess by virtue of his/her genetic and constitutional make-up.
  7. 7. Species immunity • Example: Resistance to plant pathogens and large number of animal pathogens like rinderpest and distemper. • Mechanism- unclear but may be due to physiological and biochemical differences between the tissue of different host species • Determines whether or not a pathogen can multiply in them Total or relative refractoriness to a pathogen, shown by all members of the species.
  8. 8. Racial immunity • High degree of resistance of Algerian sheep to anthrax. • In USA, people of African origin more susceptible than Causcasians to tuberculosis. • Genetic resistance to Plasmodium falciparum malaria – some parts of Africa and Mediterranean coast • Heriditary abnormality ‘Sickling’ confers immunity – survival advantage in malarial environment. Within a species, different races may show differences in susceptibility to infection. Genetic in origin, by selection and inbreeding, races possess high degrees of resistance or susceptibility to various pathogens.
  9. 9. Individual immunity • Genetic basis evident from studies on incidence of infectious disease in twins. • Ex: Homozygous twins exhibit similar degrees of resistance or susceptibility to lepromatous leprosy and tuberculosis. Difference in innate immunity exhibited by different individuals in a race.
  10. 10. Factors affecting innate immunity 1.Age: At more risk are the very young and old (Hormonal influence on resistance) - Ex 1: Tinea capitis caused by Microsporum audouinii, Spontaneous cure with onset of puberty. - Ex 2: Susceptibility of vaginal epithelium in pre-pubertal girls to gonococcal infection. - Ex 3:Poliomyelitis and Smallpox more severe in adults than in children; conversely Hepatitis B infection in newborn are usually asymptomatic because clinical disease requires adequate immune response which is lacking at that age. - However virus multiplies unrestrained and such neonates end up as chronic viral carriers and often develop late hepatic complications. - Fetus in utero protected from maternal infection by placental barrier - Except in case of some overwhelming infections like Cytomegalovirus & Toxoplasma gondii which may to lead to congenital malformations.
  11. 11. Factors affecting innate immunity 2. Hormonal influences: Enhanced susceptibility to infection. Endocrine disorders like Diabetes mellitus, adrenal dysfunction. - Ex: High incidence of staphylococcal sepsis in diabetes is attributed to increased level of carbohydrate content in the tissues. - Corticosteroids exerts an influence on the response to infection by supressing the host’s resistance by their anti-inflammatory and anti-phagocytic effects. - Steroids also supress the antibody formation and hypersensitivity. Elevated steroid level in pregnancy may lead to heightened susceptibility to many infections. - Beneficial effects by neutralising bacterial endotoxins
  12. 12. Factors affecting innate immunity 3.Nutrition: -Malnutrition: Both Humoral and Cell mediated immunity reduced. -Mantoux test done for tuberculosis becomes negative in severe protein deficiency. -Malarial infection in Famine stricken may not induce fever but once their nutrition improves, clinical malaria develops.
  13. 13. Mechanisms of innate immunity a. Epithelial surfaces: -Intact skin and mucosal membrane – mechanical barrier, bactericidal activity (due to high salt concentration in drying sweat, sebaceous secretions and long chain fatty acids and soaps). -Salmonella kept over glass slide ans skin at intervals. -Frequent mycotic and pyogenic infectionsseen in persons who immerse their hands in soap water for longer periods. - Mucosa of nose- Architecture prevents the inhaled particles entering the passage, also by mucus lining the epithelium and are swept back to the pharynx which tend to be swallowed or coughed out.
  14. 14. Mechanisms of innate immunity a. Epithelial surfaces: (CONTINUED) -Mouth (saliva); Stomach (gastric digestive juices); Conjunctiva: flushing action of lacrimal secretion. -Tears contains lysozyme, an antibacterial agent (Fleming), also present in all tissue fluids except in CSF; -Flushing action of urine eliminates bacteria from urethra. -Spermine and zinc present in sperm has antibacterial activity. -Acidity of adult vagina due to glycogen fermentation in epithelial cells by resident aciduric lactobacilli makes it inhospitable for many infections
  15. 15. Mechanisms of innate immunity b.Antibacterial substances in the blood & tissues: - Betalysin (thermostable) – active against anthrax and related bacilli - Basic polypeptides like Leukins and Plakins from Leukocytes and Platelets - Acidic substances like Lactic acid in tissues - Lactoperoxidase in milk - Interferon (Protection against viral infections)
  16. 16. Mechanisms of innate immunity - Microbial antagonism: Skin and Mucus membrane has resident commensal bacterial flora which prevent colonization by pathogens. Germ free animal (Gnotobiotic animals are susceptible to all types of infections) C. Cellular factors: Phagocytes – Metchnikoff- Phagocytosis – Microphages (Polymorphonuclear leukocytes) & Macrophages (Histiocytes-wandering ameboid cells in the tissues). -Encapsulated Streptococcus pneumoniae are not phagocytosed in the presence of opsonins. -Brucella, Salmonella typhi and Lepra bacilli resist intracellular digestion and may actively multiply inside the phagocytic cells. -NK cells activated by interferons – non-specific defense against viral infections and tumors
  17. 17. Mechanisms of innate immunity d. Inflammation e. Fever: Theraputic indication of fever was instituted in treponema pallidum infection causing Syphilis. f. Acute phase proteins: Enhance host resistance, prevent tissue injury and promote repair of onflammatory lesions. CRP, alpha-1 acid glycoprotein, serum amyloid P component, mannose binding protein, hs-crp etc. g. Toll-like receptors: Cell associated receptors in Innate immunity.
  18. 18. Innate immunity Vs Adaptive immunity
  19. 19. Innate immunity Vs Adaptive immunity
  20. 20. Adaptive immunity • Also known as Acquired immunity • Antigenic specificity • Diversity • Immunological memory • Self/non-self recognition: Self-tolerance. Failure of self tolerance results in auto- immunity
  21. 21. Types of Adaptive immunity • Active immunity • Passive immunity
  22. 22. Active immunity: • Functioning immune system – B lymphocytes – Antibody production – Production of immunologically active cells. • Sets only after latent period, often there is a negative phase where measurable immunity may be lower than it was before the antigenic stimulus. Because antigen binds to specific antibody and lower its level in circulation. • Once developed, it is long-lasting, second immune response is rapid. • Bothe CMI and humoral immunity developed; Immunological memory is present. • Active immunity more effective and confers protection than passive immunisation. Resistance developed by individual as a result of antigenic stimulus. Also called adaptive immunity
  23. 23. Natural active immunity • Clinical or inapparent infection by microbe. • Patient recovered from attack of Measles develops natural active immunity. • Large proportion to poliomyelitis due to childhood infection. • Immunity is lifelong as in Chicken pox & Measles. • Influenza or common cold; shortlived, can recur. • Premunition immunity: In Syphilis, re-infection lasts only as long the original infection remains active. Once disease is cured patient is prone for spirochete infection. • But in Chancroid, caused by Hemophilus ducreyi, no effective immunity produced, re-infection common
  24. 24. Artificial active immunity • Resistance induced by vaccines • Bacterial vaccines: Live (BCG for TB), Killed (Cholera vaccine), Subunit (Typhoid Vi antigen), Bacterial products (Tetanus toxoid). • Viral vaccines: Live (Oral polio vaccine - Sabin), Killed (Injectable polio vaccine-Salk), Subunit (Hepatitis vaccine)
  25. 25. Artificial active immunity • Live vaccines – initiate infection without causing disease or injury. Immunity lasts for several years, but booster dose necessary. Can be administered orally or parenterally. • Killed vaccines – Less immunogenic than live vaccines. Protection lasts only for a short period. Atleast 3 doses required 1. Primary dose, 2. booster dose. Ideal route: Parenteral. May be given orally, but not effective. • Humoral antibody response following parenteral immunisation can be improved by adding ‘adjuvants’ like Aluminium phosphate.
  26. 26. Passive immunity: • No active role from host’ immune system. No need antigenic stimulus. Preformed antibodies are administered. • No latent period. Immediately after administration, renders active protection. • No negative phase. No secondary IR. • Immunity is transient, lasting days to weeks, only till the passively transmitted antibodies are metabolised and eliminated. • Factor of Immune elimination limits the usefulness of repeated passive immunisation. • Less effective, acts immediately so it provides ‘instant immunity’ Resistance transmitted passively to a recipient in ready made form.
  27. 27. Types of Passive immunity • Natural passive immunity • Artificial passive immunity • Combined immunisation
  28. 28. Natural passive immunity • Resistance passively transferred from mother to baby. • Maternal antibodies are transmitted to baby by placenta. • Human colostrum- rich in IgA, resistant to intestinal digestion, gives protection to the neonates. • Human fetus, by 20th week starts producing IgM but still inadequate at birth. • By 3 months of age- infant acquires some immunological independence, though maternal antibodies give passive protection. • Active immunisation of mothers during pregnancy can improve the quality of passive immunity in infants.
  29. 29. Artificial passive immunity • Resistance transferred to a recipient by administration of antibodies. • Hyperimmune serum of humans or animals • Convalescent sera and pooled human gamma globulin. • Equine hyperimmune sera such as anti-tetanic serum (ATS) prepared from hyperimmunised horses was extensively employed but now stopped due to hypersensitivity reactions and immune elimination.
  30. 30. Artificial passive immunity • Human hyperimmune globulin such as Tetanus Immune Globulin (TIG) free from those complications and provides more lasting protection. • Animal preparations (antisera) like anti-gas gangrene, anti-venom & anti-botulinum preparations are used due to non-availability of human preparations. • Convalescent sera (Acute phase serum and serum obtained from patients recovering from infectious diseases) contains high level of specific antibody. • Pooled human gamma globulin (from healthy adults) contains antibodies against common pathogens prevalent in the region. • Convalescent sera and pooled immune globulin is used for passive immunisation against some viral hepatitis A infections.
  31. 31. Artificial passive immunity • Human gamma globulin is used in treatment of patients with immunodeficiencies. • Indications: • For immediate and temporary protection in a non-immune host faced with threat of infection. • To suppress active immunity if it is injurious, for ex: rh immune globulin during delivery to prevent IR to rhesus factor in Rh negative women with Rh positive babies.
  32. 32. Combined immunisation • Non-immune individual with a teatanus prone wound is treated by combined immunisation where both active and passive immunisation used. • Passive immunisation provides immediate protection. • Method: inject TIG in one arm and first dose of tetanus toxoid in the other.Followed by full course of phased teatanus injections. • TTG gives protection till active immunity is able to take effect.
  33. 33. Active immunity Vs Passive immunity Active immunity Passive immunity a. Produced actively by the host’s immune system a. Received passively. No active host participation b. Induced by infection or by immunogen b. Readymade antibody transferred c. Durable effective protection c. Transient, less effective d. Immunity effective only after lag period d. Immediate immunity e. Immunological memory present e. No immunological memory f. Booster effect on subsequent dose f. Subsequent dose less effective g. Negative phase may occur g. No negative phase h. Not applicable in the immunodeficient h. Applicable in the immunodeficient
  34. 34. Adoptive immunity • A special type of immunisation by the injection of immunologically competent lymphocytes. • Whole lymphocytes or a part called ‘transfer factor’ can be used. • Ex: Lepromatous leprosy treatment.
  35. 35. Measurement of immunity • Resistance of an individual to a challenge by pathogen is difficult to measure. • Accurate measurement not possible, so statistical methods used. a. Demonstration of specific antibody by agglutination, precipitation, complement fixation test, hemagglutination inhibition, neutralisation test, ELISA and others. b. In-vitro or in-vivo methods in case of diphtheria, Schick test (Toxin assay) c. Skin tests for delayed hypersensitivity and in-vitro tests for CMI
  36. 36. Local immunity • Besredka proposed this concept • Local site or at site of primary level of entry of the infectious pathogen – target. • Ex 1: In Poliomyelitis-Systemic immunity achieved by active immunisation with killed vaccine, but local intestinal or gut immunity is achieved by natural infection or by live oral immunisation. • Ex 2: Influenza, humoral immunity elicited by killed vaccine, but natural infection or intranasal live virus vaccine provides local immunity. • IgA (Secretory IgA produced locally by Plasma cells)– special class of immunoglobulin confers local immunity by mucosal or secretory system.
  37. 37. Herd immunity Herd- Large proportion of individuals in a community Infectious pathogen causing communicable disease Potential to cause epidemic in susceptible individuals
  38. 38. Herd immunity Herd immunity (Satisfactory): Large proportion of susceptible population in the Community are immune to the disease causing pathogen Herd immunity (Low): Epidemics are likely to occur To eradicate a communicable disease: Herd immunity is important than individual immunity
  39. 39. SUMMARY & TAKE HOME MESSAGE
  40. 40. THANK YOU

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