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IMMUNITY Babitha Elias DEFINITION Immunity refers to the resistance exhibited by the host towards injury caused by microorganisms and their products. Types of immunity INNATE IMMUNITY Definition: Resistance to infections which an individual possesses by virtue of his genetic and constitutional make-up. It is not affected by prior contact with microorganisms or immunisation. It is non specific. I. INNATE IMMUNITY Types of innate immunity Species Racial Individual Species immunity: total or relative refractoriness to a pathogen, shown by all members of a species. Eg: human spp are resistant to plant pathogens Racial immunity: Within a species, different races may show resistance in susceptibility to infections. Eg: Resistance of Algerian sheep to anthrax. Resistance of Caucasians to Tb Individual immunity: the differences in innate immunity exhibited by different individuals in a race. Eg: innate immunity in Twins. FACOTRS THAT INFLUENCE THE INNATE IMMUNITY Age Hormones Nutrition AGE Extremities of age is susceptible to infection. Fetus in utero – protected by the placental barrier. Congenital malformations can occur if the pathogens cross the placental barrier – Eg: Toxoplasma, Rubella, Cytomegalovirus, Herpes infections. Susceptibility in the young – hormonal influence. Eg: Tinea capitis, gonorrhea in prepubertal girls Some infections are severe in adults due to hypersensitivity. Eg: Poliomyelitis, Chickenpox. Some infections are asymptomatic in newborn – lack of adequate immune response. Eg: Hepatitis B HORMONAL INFLUENCES Endocrine disorders like diabetes mellitus, hypothyroidism, adrenal dysfunction – increased susceptibility to infection. Corticosteroids – Depress the host’s resistance by antiinflammatory, anti-phagocytic effects, suppression of Ab formation and by hypersensitivity. Elevated steroid level in pregnancy - increase susceptibility. NUTRITION Malnutrition predisposes to bacterial infections. Some infections may not become clinically apparent in severely malnourished. Eg: malaria. MECHANISMS OF INNATE IMMUNITY Epithelial surfaces Antibacterial substances in blood & tissues Cellular factors in innate immunity. Inflammation Fever Acute phase proteins Epithelial surfaces Intact skin & mucous membrane covering the body – gives protection against invasion of microbes. Skin Possesses bactericidal activity. Sweat, sebaceous secretions provide protection. Normal flora of skin Resident flora – group of organisms present on the skin which are not easily removed by washing and disinfectants. Transient flora – bacterial flora which is easily removed by washing & disinfectants. Normal flora - prevent colonisation by pathogens. of normal resident flora – lead to invasion of microbes Alteration Eg: Staphylococcal or Clostridial enterocolitis following oral antibiotics. Respiratory tract: Architecture of nose Nasal & respiratory secretions Ciliary action Cough reflex Intestinal tract: Saliva Acidity of stomach Gastric juices Normal flora – prevent colonisation of pathogens Conjunctiva: Flushing action of tears. Lysozyme in the tears. Genitourinary tract: Flushing action of urine. Acidic pH of vaginal secretions. Spermin from semen. Antibacterial substances in blood & tissues Complement Properdin Beta lysin Leukins & plakins Lysozyme Interferon against viral infections Cellular factors in innate immunity cells – microphages & macrophages Natural Killer (NK) cells Phagocytic Phagocytosis Metchnikoff (1883) Phagocytosis is a process by which the microorganisms are ingested and destroyed by the phagocytic cells. Microphages – polymorphonuclear leukocytes (Neutrophils) Macrophages – histiocytes (tissue) & monocytes (blood) Steps in phagocytosis 1. Chemotaxis 2. Adherence 3. Ingestion 4. Intracellular killing Inflammation Tissue injury or irritation initiated by the entry of pathogens or other irritants leads to inflammation. Inflammation leads to vasodilation, increased vascular permeability, cellular infiltration. Microorganisms destroyed. are phagocytosed & There is outpouring of plasma, which helps to dilute the toxic products present. A fibrin barrier is laid. Inflammation Redness Heat Swelling Pain is characterized by Fever Rise It in temperature following infection. accelerates the physiological processes. Sometimes Stimulates destroy the pathogens. the production of interferons. Acute phase proteins Infection or injury leads to sudden increase in plasma concentrations of certain proteins – Acute phase proteins. They include C reactive protein (CRP), mannose binding protein. They enhance host resistance, activate alternate pathway of complement, prevent tissue injury, promote repair of inflammatory lesions. ACQUIRED IMMUNITY DEFINITION The specific resistance acquired by an individual during life. II. TYPES OF ACQUIRED (ADAPTIVE) IMMUNITY Natural (clinical/subclinical infection) a) Active Artificial (vaccination) Natural (mother to child) b) Passive Artificial (antiserum) ACTIVE IMMUNITY DEFINITION: Active immunity is the specific resistance against an infection which develops after exposure to immunogen. Produced actively by the immune system. Develops after a latent period – required for the immune system to act. Immunity is long lasting. Mechanism of active immunity 2 Mechanisms: I. Humoral immunity II. Cell mediated immunity Humoral immunity (Antibody mediated) It depends on the synthesis of Antibodies by plasma cells. Plasma cells – which produce & secrete antibodies specifically against the antigen The specific antibodies produced provide resistance by the following mechanism: Neutralization i) Specific Abs produced against toxins are called antitoxins, which neutralize the toxin & give protection against toxic bacterial infection. Eg: Tetanus, Diphtheria ii) Specific Abs produced against infectious agents can neutralize a pathogen Eg: Neutralizing Abs against viruses. Opsonisation Ab produced against an infectious agent could act as an OPSONIN which can enhance adherence of infectious agent onto the phagocyte & enhances phagocytosis. Complement fixation Ab can activate complement by classic pathway. After the activation of complement, it mediate mechanisms such as opsonisation, chemotaxis & cell lysis. CELL MEDIATED IMMUNITY (CMI) Cell mediated immune response depends on T – lymphocytes developed against certain antigens. CMI gives protection against viral, parasitic, fungal & intracellular bacterial infections – tuberculosis, leprosy etc. TYPES OF ACTIVE IMMUNITY 1. Natural Active immunity It is the specific resistance an individual develops after infection – either clinical or sub-clinical infection. Immunity is long lasting. Eg: Chickenpox, Mumps & measles. Immunity may be short lived – Eg: Influenza, common cold Artificial Active immunity It is the specific resistance which develops in an individual after vaccination. Vaccines – are preparations which consists of live attenuated or killed microorganisms or toxoids used for immunization purposes. Live attenuated vaccines: Attenuation : is a process by which the virulence of an organism is reduced without altering the immunogenicity. 2. Attenuation is done by growing the microorganisms at unfavorable conditions. Eg: BCG vaccine for tuberculosis Ty 21a vaccine for typhoid Sabin vaccine for poliomyelitis MMR vaccine for Mumps, measles, rubella 17D vaccine for yellow fever Killed vaccine The organisms are killed by heat, formalin, phenol & alcohol. These are preserved in phenol or alcohol. Eg: TAB vaccine for enteric fever Salk vaccine for poliomyelitis Antirabies vaccine Toxoids: Toxoids are inactivated exotoxins which has lost its toxicity but has retained its immunogenicity. Used to immunize against bacterial infections – diphtheria & tetanus. Eg: DPT vaccine PASSIVE IMMUNITY DEFINITION: Specific resistance which develops in an individual after receiving preformed antibodies. The antiserum is prepared by injecting infective agent or toxin in another host. Immune system has no active role. Protection starts immediately after the administration of antiserum. No latent period. Immunity is short lasting. TYPES OF PASSIVE IMMUNITY Natural Artificial Natural passive immunity Specific resistance which a child receives from mother through placenta or through milk. Clinical significance Protects the child from many infections Eg: Rota virus diarrhoea Active immunization of pregnant female with Tetanus toxoid will immunize the mother & protects the child from neonatal tetanus. Artificial passive immunity Develops in an individual following administration of antisera or immunoglobulin The source of the antisera may be animal or human origin, convalescent sera, pooled gammaglobulin. Animal sera Prepared by immunizing horse with toxoid. Eg: Anti-tetanus serum (ATS) Anti-diphtheria serum (ADS) Disadvantages: 1. As animal sera is foreign protein – causes hypersensitivity reactions in humans. of immune elimination – the specific Abs formed will combine with the antisera given subsequently & get eliminated quickly 2. Risk Human antisera Prepared by hyperimmunisation of human volunteers with toxoid. Protection with human antisera lasts longer & there is no immune elimination. Convalescent sera Sera of patients recovering from infectious diseases. Eg: Used against Measles & Rubella. Pooled human gammaglobulin Prepared by using sera of healthy individuals. Eg: For viral hepatitis A Uses of Passive immunity 1. Provide immediate short term protection in a non-immune host. 2. For the suppression of active immunity which may be injurious – Eg: for Rh incompatibility 3. For the treatment of serious infections. Differences between Active & Passive immunity Features Contact with immunogen Lag period Active immunity Passive immunity Yes No Present Absent Long lasting Short Present Absent Negative phase Present Absent Usefulness in immunodeficient host No Yes Duration of protection Memory Local immunity It is the resistance an individual has at the site of entry of pathogen. Provided by secretory Ig A. Eg: Oral polio vaccine. Herd immunity It refers to overall resistance in a community. Eg: OPV Eradication of any communicable disease depends on development of high level of herd immunity