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Immunity
The document discusses the two main types of immunity: innate and acquired, detailing their mechanisms and factors affecting individual susceptibility to infections. It describes how innate immunity is present from birth and includes species, racial, and individual immunity, while acquired immunity can be active or passive, developed through exposure to antigens or transferred from another individual. The summary also covers the roles of phagocytosis, inflammation, fever, and various immune responses in protecting against pathogens.
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Immunity
- 1.
- 2. Definition Resistance exhibited bythe host towards injury caused by microorganism & their products Immunity is concerned with reaction of body against any foreign antigen
- 3. Types Immunity against infectiousdiseases is of different types Innate (native) immunity Non-specific Species Racial Individual Specific Species Racial Individual
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- 5. Innate immunity Resistance toinfections that an individual possesses by virtue of his genetic constitutional make-up Immunity present since birth (inborn) It is not affected by prior contact with microorganisms or immunisation Non-specific: degree of resistance to infections in general Specific: resistance to particular pathogen
- 6. Species immunity: Total orrelative resistance to pathogen, shown by all members of species Eg: All human beings are resistant to plant pathogens & many animal pathogens Mechanism is not clearly understood but may be due to physiological & bichemical differences between tissues of different species 3 levels of innate immunity: species, racial, individual
- 7. Racial immunity: Different raceswithin same species may show differences in susceptibility to infection Eg: high resistance of Algerian sheep to anthrax Another example: genetic resistance to Plasmodium falciparum in some parts of Africa Racial differences are genetic in origin, by selection & inbreeding
- 8. Individual immunity: Difference inimmunity exhibited by different individuals in race It is well documented that homozygous twins show similar degrees of susceptibility to leprosy & TB This immunity is due to genetic constitution of individual
- 9. Factors affecting individualinnate immunity 1. Age: Very young & very old: more susceptible to infectious disease Fetus in uterus is protected from maternal infection by placental barrier. But some pathogens cross the barrier causing overwhelming infection resulting in fetal death Some infections are more severe in adults than in young children due to hypersensitivity Old persons are highly susceptible to infections due to declined immune responses
- 10. 2. Hormonal influence: Endocrinedisorders (diabetes, hypothyroidism, adrenal dysfunction) are associated with enhanced sensitivity to infections High incidence of staphylococcal sepsis in diabetes: due to increased level of carbohydrates in tissues Corticosteroid hormones have anti-inflammatory & anti-phagocytic effect: depress host’s resistance Elevated steroid level during pregnancy: hightened susceptibility to many infections
- 11. 3. Nutrition: Malnutrition: reducedcell mediated & humoral immunity Cell mediated immune responses decrease in severe protein deficiency
- 12. Mechanisms of innateimmunity 1. Epithelial surface: Skin & mucus membrane covering body protect it against invasion by microorganisms Skin: Mechanical barrier Possesses bactericidal activity due to high salt concentration in drying sweat, sebaceous secretions & long chain fatty acids Normal flora on skin: prevents colonisation by pathogens
- 13. Respiratory tract: Inhaled particlesare arrested in nasal passages on moist mucus membrane surface Pathogens are trapped by mucus lining epithelium & given to pharynx where they are swallowed or coughed out Cough reflex: important defense mechanism Nasal & respiratory secretions contain mucopolysaccharides that combine with influenza & other viruses Particles that reach alveoli are ingested by phagocytic cells
- 14. Digestive tract: Mouth saliva:inhibitory effect on many microbes Swallowed pathogens: destroyed by acidic pH of gastric juice Normal flora of ileum inhibits growth of pathogens Conjunctiva: Tear secretion flush away bacteria & other foreign particles Tear contains antibacterial lysozyme: break down polysaccharide of bacterial cells
- 15. Genitourinary tract: Flushing actionof urine: eliminates bacteria from urethra Spermine & zinc in semen: antibacterial activity Acidic pH of vaginal secretions in females, due to fermentation of glycogen by lactobacilli, inhibit pathogens
- 16. 2. Antibacterial substancesin blood & tissues: Complement system: bactericidal activity & result in destruction of pathogenic bacteria Antibacterial substances: beta lysin, leukins, plakins, lactic acid, lactoperoxidase, lysozyme Interferons produced by cells: antiviral activity
- 17. 3. Cellular factors: Pathogensinvading blood & tissue: destroyed by phagocytic cells Phagocytes: microphages & macrophages Microphages are polymorphonuclear leucocytes Macrophages are wandering amoeboid cells in tissues, reticuloendothelial cells & monocytes in blood
- 18. Phagocytic action ofphagocytes is divided in 4 stages: Chemotaxis: Phagocytic cells attracted by chemotactic substances → reach site of inflammation Attachment: Infective agent gets attached to phagocytic membrane Ingestion: Bacteria are engulfed by phagocytes Membrane of phagosome fuses with lysosome to form phagolysosome
- 19. Intracellular killing: Lytic enzymesin phagolysosome destroy bacteria Some bacteria (mycobacteria) resist such killing & can multiply within phagolysosome A class of lymphocyts called Natural killer (NK) cells play important role in non-specific defence against viral infections & tumor
- 21. 4. Inflammation: Entry ofpathogens → tissue injury & irritation → leads to inflammation Inflammation leads to vasodilation, increased vascular permiability & cellular infiltration Arterioles at the site of infection constrict initially & then dilate leading to increased blood flow → leucocytes escape into tissues by diapedesis → accumulate in large numbers → attracted by chemotactic substances at site of injury → phagocytose microbes
- 22. Inflammation is characterisedby: Pain (Dolor), Redness (Rubor), Heat (Calor), Swelling (Tumor) Plasma helps in diluting toxic products Fibrin barrier forms wall around site of infection
- 23. 5. Fever: Rise intemperature after infection: helps to accelerate physiological processes Fever stimulates production of interferons & helps in recovery from viral infections 6. Acute phase proteins: Infection or injury leads to sudden increase in concentration of certain proteins: called Acute phase proteins Eg: C ractive protein (CRP), alpha-1-acid glycoprotein, mannose binding protein
- 24. Acquired immunity Resistance thatan individual acquires during life Two types: o Active immunity o Passive immunity Active immunity: Resistance developed by individual as a result of antigenic stimulus Involves active functioning of host’s immune apparatus to produce antibodies & immunologically active cells
- 25. Active immunity setsin after a latent period During its development, there is often a negative phase (immunity lower than it was before antigenic stimulus): because Ag combines with pre-existing Ab in circulation Once developed, it is long-lasting When actively immunised individual encounters subsequent attack of same Ag, immune response occurs more quickly (called as secondary response) Besides cell mediated & humoral immune response, it is also associated with immunological memory Active immunisation is more effective & confers better protection than passive immunisation
- 26. Passive immunity: Resistance transmittedpassively to recipient in a readymade form Recipient’s immune system plays no active role There is no antigenic stimulus; instead, preformed Ab are administered No latent period No negative phase Immunity is transient lasting for days or weeks
- 27. No secondary typeresponse occurs in this immunity. When Ab is administered 2nd time, they are eliminated more rapidly Passive immunisation is less effective Employed when instant immunity is desired
- 28. Both Active &Passive immunities are further classified as Natural & artificial Natural active immunity: Results from either clinical or inapparent infection by a microbe Eg: person recovered from attack of measles develops natural active immunity Such immunity is usually long-lasting but duration varies with types of pathogen Immunity is lifelong following many viral diseases Immunity following bacterial infection is generally less permanent
- 29. Artificial active immunity: Resistanceinduced by vaccine Examples of vaccines: Bacterial vaccines: o Live (BCG for tuberculosis) o Killed (Cholera vaccine) o Subunit (Typhoid Vi antigen) o Bacterial products (Tetanus toxoid) Viral vaccines: o Live (Oral polio vaccine- Sabin) o Killed (Injectable polio vaccine- Salk) o Subunit (Hepatitis B vaccine)
- 30. Live vaccines initiatean infection without causing any injury or disease Immunity following live vaccine administration resembles that following natural infection Immunity lasts for several years but booster doses may be required Live vaccines can be administered orally or parenterally Killed vaccines are less immunogenic than live vaccines, & protection lasts for short period. Thus, administered repeatedly
- 31. Natural passive immunity: Resistancepassively transferred from mother to baby In human infants, maternal Ab are transmitted predominantly through placenta In animals such as pigs, Ab are transmitted through colostrum Human fetus acquires ability to produce antibodies from 20th week of life. Till then, maternal Ab give passive protection against infectious diseases
- 32. Artificial passive immunity: Resistancepassively transferred to recipient by administration of Ab Agents used for this purpose: - Hyperimmune sera of animal or human origin - Convalescent sera - Pooled human gammaglobulin These are used for prophylaxis & therapy
- 33. Hyperimmune sera: Antitetanus serumprepared form hyperimmune horses Give temporary protection Disadvantage: hypersensitivity & immune elimination Human hyperimmune globulin: more lasting protection Convalescent sera: Sera of patients recovering from disease Contains high levels of specific Ab
- 34. Pooled human gammaglobulin: Gammaglobulinfrom pooled sera of healthy individuals Contains Ab against all common pathogens prevalent in the region
- 35. Active immunity Passiveimmunity Produced actively by host’s immune system Received passively. No active host participation Induced by infection or by immunogens Readymade Antibody transferred Durable effective protection Transient, less effective Immunity effective only after lag period Immediate immunity Immunological memory present No memory Booster effect on subsequent dose Subsequent dose less effective Negative phase may occur No negative phase Not applicable in immunodeficient Applicable in immunodeficient