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BY- DR. MANISH TIWARI
TUTOR MICROBIOLOGY
SMC(UNNAO)
IMMUNITY
 Is the state of having sufficient biological defenses to avoid infection,
disease, or other unwanted biological invasion.
 This state of protection has both less specific and more specific
component.
 It is the capability of the body to resist harmful microbes
from entering into the body.
WHAT ARE THE IMMUNE SYSTEM?
 isa system of biological structuresand processes within an
organism that protects againstdisease.
 Tofunction properly, an immunesystem mustdetectawide
variety of agents, from viruses to parasitic worms, and
distinguish them from theorganism'sown healthytissue.
 The immunesystem recognizes foreign bodies and responds with
the productionof immunecellsand proteins
 Barriers helpan organism todefend itself from the many
dangerous pathogens it mayencounter
How is the immune system activated?
 The immune system can be activated by a lot of different things
that the body doesn’t recognize as its own.
 These are called antigens. Examples of antigens include the
proteins on the surfaces of bacteria, fungi and viruses.
 When these antigens attach to special receptors on the immune
cells, a whole series of processes are triggered in the body.
 Once the body has come into contact with a disease-causing
pathogens for the first time, it usually stores information about
the pathogens and how to fight it.
 Then, if it comes into contact with the pathogens again, it recognizes
the pathogens straight away and can start fighting it faster.
 The body’s have proteins on their surface, too. But those proteins
don’t usually trigger the immune system to fight the cells.
 Sometimes the immune system mistakenly thinks that the body's
own cells are foreign cells. It then attacks healthy, harmless cells in
the body. This is known as an autoimmune response.
Importance of the immune system
 Without an immunity, we would have no way to fight harmful
things that enter our body from the external environment or
harmful changes that occur inside our body. The main tasks of
the immunity are….
 to fight disease-causing germs (pathogens) like bacteria,
viruses, parasites or fungi, and to remove them from the body,
 to recognize and neutralize harmful substances from the
environment, and to fight disease-causing changes in the body,
such as cancer cells.
How does the immunity work?
 The immunity has a vital role: It protects your body from harmful
substances that could make you ill.
 It is made up of various organs, cells and proteins.
 As long as your immune system is running smoothly, you don’t
notice that it’s there. But if it stops working properly – because it’s
weak or can't fight particularly aggressive pathogens – you get ill.
 Pathogens that your body has never encountered before are also
likely to make you ill.
 Some pathogens will only make you ill the first time you come into
contact with them. These include childhood diseases like
chickenpox.
CLASSIFICATION
1. INNATE IMMUNITY
 nonspecific immunity
 is the natural resistances with which a person is born.
 It provides resistances through several physical, chemical
and cellular approaches.
 Microbes first encounter theepithelial layers, physical
barriers that line skin and mucousmembranes.
 Subsequent general defenses include secreted chemical
signals (cytokines), antimicrobial substances, fever, and
phagocytic activity associated with the inflammatory
responses.
 The phagocytes express cell surface receptors that can bind and
respond to common molecular patterns expressed on the surface
of invading microbes.
 Through these approaches, innate immunity can prevent the
colonization, entry and spread of microbes.
INNATE IMMUNITY
• Recognition of traits shared by
broad ranges of pathogens,using
a small set ofreceptors
• Rapid response
ACQUIRED IMMUNITY
• Recognition of traits specific to
particular pathogens, using avast
array of receptors
• Slowerresponse
Barrierdefenses:
Skin
Mucous membranes
Secretions
Internal defenses:
Phagocytic cells
Antimicrobial proteins
Inflammatory response
Natural killercells
Humoral response:
Antibodies defendagainst
infection in bodyfluids.
Cell-mediated response:
Cytotoxic lymphocytes defend
against infection in bodycells.
Pathogens
(microorganisms andviruses)
FEATURES
 Acts in the minute:- is the 1st line of host defence against
infection.
 Prior microbial exposure is not required.
 Diversity is limited:- it is active only against a limited repertoire
of antigen.
 Non specific:- it can directed against any microbial antigen, not
for particular.
 No memory :- it does not have a memory component.
 Note :- innate immunity may be considered at the level of the
species, races or individual.
1. Species immunity: is the innate immunity towards a microbes
exhibited by all members of given species,e.g , frogs are
resistant to bacillus anthracis; while towards are susceptible.
2. Racial immunity: some time innate immunity is confined to a
particular race; which may be absent in the other
communities. E.g. negroes of America are more susceptible
to tuberculosis than the white.
3. Individual immunity: it is refer to the antimicrobial defense
mechanisms that are confined to a particular individual.
FACTORS INFLUENCING INNATE IMMUNITY
1. Age :
 In fetus 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
MECHANISM OF INNATE IMMUNITY:
 1. Epithelial surface:
 a. Skin:
 It acts as a machanical barrier to microorganisms and provide
bactericidal
 secretions
 Resident microflora of skin and mucous membrane suface help
to prevent
 colonisation by pathogens
 Altertation of normal resident flora may lead to invasion by
extraneous microbes and thus causing serious disease. e.g
Clostridial enterocoloitis fallowing oral antibiotics
 b. Resiratory tract:
 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
 c. Intestinal tract:
 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 uretar
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.
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.
Phagocytic cells are classified as:
i) Microphages e.g.
polymorphomucleraleucocytes (
neutrophils)
ii) Macrophages e.g mononuclear
phagocytic cells
Immunity lecture
 Phagocytic action are
divided into 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 hydrolytic
enzymes of lysosomes
 Natural killer cells play a important role in non specific
defence against viral infections and tumour.
4. INFLAMMATION:
 Inflammation occurs as 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
Immunity lecture
5. FEVER:
 Rise of temperature fallowing infection is a natural
defence mechanism.
 It destroyes the infecting organisms.
 Fewer also stimulates the production of interferon which
helps in recovery from viral infection.
2. ACQUIRED IMMUNITY
 Acquired immunity is defined as the resistant against
the infecting foreign substance that an individual
adapts during the course of his life.
 Not related to innate immunity
FEATURE
 Mediators :T cells & B cells it is chief mediators of acquired
immunity. And other mediators such as:
 Classical complement pathway.
 Antigen presenting cells (APC).
 Cytokine such as IL2, IL4 & IL5.
 Response occurs in day.
 Requires prior microbial exposure : it develops only after
exposure to the microbes.
 It is not present prior to the 1st contact with the microbes.
 Specific : highly specific
 Memory cells present.
 Diversity is wide:
 Host cells receptors : it is specific for particular microbial
antigen. Example T cells receptors , B cells receptors &
immunoglobulin receptors.
Immunity lecture
Active immunity VS. Passive immunity
Innate immunity VS. Acquired immunity.
Immunity lecture
ACQUIRED ACTIVE IMMUNITY
Resistance developed as a result of antigenic stimulus
Also called “Adaptive Immunity
Active involvement of host immune apparatus
Leads to production of antibodies / Immunologically active
cells
Takes time to set in after infection
 Initial NEGATIVE PHASE : The level of measureable
immunity is lower than it was before exposure to antigen.
The antigen combines with the existing antibody leading to
reduction in existing levels of antibody.
Once active immunity sets in
It is long lasting
One second exposure to same antigen the immune response is
quick and abundant
Development of humoral & cellular immunity
Immunological memory
 Active immunization is more effective and confers better
protection
May be Natural orArtificial
NATURALACTIVE IMMUNITY
 May be as a result of clinical or inapparentinfection
 Measles infection gives the patient life longimmunity
 Adults in developing countries have natural active immunity
against polio because of inapparent infections inchildhood
 Duration of immunity depends on the pathogen
 Short term – Eg. Influenza
 Long term - Eg. Measeles , chicken pox
 Bacterial infections provide with less degree of
immunity
 PREMUNITION – Seen in syphilis . The immunityto
reinfections lasts only till the original infection is active.
 Chancroid does not provide the person with any
immunity . Person may develop lesionsfollowing
reinfection even when original infection isactive.
ARTIFICIALACTIVE IMMUNITY
• Resistance induced by vaccines
• Vaccines are preparations of live or killed microorganisms or
their products used for immunization
• Bacterial vaccines
– Live : BCG vaccine
– Killed: Cholera vaccine
– Subunit : Typhoid Vi antigen
– Bacterial products: Tetanus toxoid
• Viral vaccines
– Live : OPV-Sabin
– Killed : IPV – Salk
– Subunit : Hepatitis B Vaccine
VACCINES
 LIVE VACCINES
• Infection without disease
• Immunity lasts for several
years
• Booster doses MAYBE
needed
• Can be given orally or
parenterally
 KILLED VACCINES
• No infective stage
• Less immunogenic
• Repeated doses needed
– Primary dose
– Booster dose
• Oral doses not effective
• Parenteral doses given with
adjuvant to increase humoral
immunity
PASSIVE IMMUNITY
 No infection
 Readymade antibodiesare
administered
 No latent period
 No negative phase
 Immediate protection
 Immunity lasts for short duration
till antibodiesare metabolized
 No secondary response
 Passive immunity decreases with
repetition
NATURAL PASSIVEACQUIREDIMMUNITY
Resistance transferred from mother to baby
Via placenta
Breast milk – colostrum – IgA
IgM production by fetus can start from 20th week of
intrauterine life
Inadequate immunity at birth
By 3 months of age – immunological independence
• < 3 months – Pediatric infections are common
Active immunization of mother provides passive immunity
to infants
 Eg. Tetanus toxoid during pregnancy
ARTIFICAL PASSIVEACQUIRED IMMUNITY
 Resistance transferred by administration of antibodies
1. Hyper immune sera
2. Convalescent sera
3. Pooled human Ɣ globulin
 Used for prophylaxis and therapy
HYPERIMMUNE SERA
• Anti-tetanus serum (ATS)
• Prepared from hyperimmunized horses
• Temporary protection
• Disadvantages
• Hypersensitivity
• Immune elimination
• In use
 – Hyperimmune globulin of human origin
CONVALESCENT SERA
 Sera of patients recovering from disease
 Contain high levels of antibody specific to the disease
 Use – Viral infections like HepatitisA
 Pooled human Ɣ globulin
 Ɣ globulin from pooled sera of healthyadults
 Has antibodies to all pathogens prevalent in thearea
 Use – Rx of patients with immunodeficiencies
INDICATIONS FOR PASSIVE IMMUNIZATION
• Immediate and temporary protection of a person at risk of
developing infection
• Toarrest overactive active immunity
 Eg. Rh incompatibility
Combined immunization
 Combination of active and passive methods
 Passive immunization for immediate protection
 Tetanus
 TIG in one arm + TT in other arm
 Followed by complete schedule of tetanus vaccination
Adoptive immunity
 Special type of immunization
 Injection of immunologically competent lymphocytes
TRANSFER FACTOR
 Tried in treatment of Lepromatous Leprosy
Local immunity
• it is mediated by a type of IgA antibody called secretory IgA which prevent the
entry of microbes at the local site itself.
• Treatment of infections in a localized area
• Polio –
– Systemic immunity by IPV
• Does not prevent multiplication of virus in thegut
– This is achieved by OPV
• Influenza
– Killed vaccine brings about a humoral response
• Not enough to prevent infection
• Intra nasal live virus injection/ natural infectionprovides local
immunity
– IgA
Immunoglobulin A (IgA)
• Secretory IgA
• Produced locally by plasma cells on mucosal surfaces /
Secretory glands
• With exposure to an antigen Specific
IgA is produced
• Mucosal defense
• Handling of antigens contracted from food and external
environment
Herd immunity
 Overall immunity in a community
 Useful in control of epidemics
 When LARGE NUMBER of people in a community are
immune to a specific pathogen Herd immunity is
SATISFACTORY
 Eradication of communicable disease lies in development of
good herd immunity rather than developing individual
immunity
How to measurement of immunity
 Practically not possible to measure accurately
 Simple method is to demonstrate the presence of a
specific antibody
– Not reliable as one pathogen will illicit immune response to
multiple antigens
 Antibody demonstration
– Agglutination
– Precipitation
– Complement fixation
CONTI…..
– Hemagglutination inhibition
– Neutralization
– ELISA
 If antigenic component is identified in-vitro or in-vivo
assays can be done.
If immunity is associated with cell mediated immunity
– Skin tests for delayed hypersensitivity
– In-vitro tests for Cell mediatedimmunity
1.MCQ
1.Which of the following statement is false about active immunity?
a) Immunological memory is present
b) Produced by host immune system
c) Immunity develops immediately
d) It is effective only after short period
2. Memory cells present in(…..)
a) Active immunity
b) Passive immunity
c) Both
d) Non of these
3. Innate immunity contain all cells except:
a) N. K cells.
b) Dendritic cells
c) Mast cells
d) B cells
4. Example of killed vaccine?
a) BCG
b) Typhoid Vi antigen
c) Cholera vaccine
d) Non of these
5. Which type of antibody found in breast milk?
a) IgM
b) IgG
c) IgA
d) IgE
6. N. K cells component of:
a) Innate immunity
b) Acquired immunity
c) Active immunity
d) Passive immunity
7. Phagocytic cell is component of:
a) Adaptive immunity
b) Innate immunity
c) Both
d) Non of these
8. Which of the following about passive immunity is true?
a) Memory cells present
b) Memory cells absent
c) It produced due to contact with antigen
d) More effective in protection
2.WRITE A SHORT NOTE :
1. What is Immunity? Briefly describe acquired immunity.
2. Herd immunity.
3. Acquired immunity.
THANK YOU!

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Immunity lecture

  • 1. BY- DR. MANISH TIWARI TUTOR MICROBIOLOGY SMC(UNNAO)
  • 2. IMMUNITY  Is the state of having sufficient biological defenses to avoid infection, disease, or other unwanted biological invasion.  This state of protection has both less specific and more specific component.  It is the capability of the body to resist harmful microbes from entering into the body.
  • 3. WHAT ARE THE IMMUNE SYSTEM?  isa system of biological structuresand processes within an organism that protects againstdisease.  Tofunction properly, an immunesystem mustdetectawide variety of agents, from viruses to parasitic worms, and distinguish them from theorganism'sown healthytissue.  The immunesystem recognizes foreign bodies and responds with the productionof immunecellsand proteins  Barriers helpan organism todefend itself from the many dangerous pathogens it mayencounter
  • 4. How is the immune system activated?  The immune system can be activated by a lot of different things that the body doesn’t recognize as its own.  These are called antigens. Examples of antigens include the proteins on the surfaces of bacteria, fungi and viruses.  When these antigens attach to special receptors on the immune cells, a whole series of processes are triggered in the body.  Once the body has come into contact with a disease-causing pathogens for the first time, it usually stores information about the pathogens and how to fight it.
  • 5.  Then, if it comes into contact with the pathogens again, it recognizes the pathogens straight away and can start fighting it faster.  The body’s have proteins on their surface, too. But those proteins don’t usually trigger the immune system to fight the cells.  Sometimes the immune system mistakenly thinks that the body's own cells are foreign cells. It then attacks healthy, harmless cells in the body. This is known as an autoimmune response.
  • 6. Importance of the immune system  Without an immunity, we would have no way to fight harmful things that enter our body from the external environment or harmful changes that occur inside our body. The main tasks of the immunity are….  to fight disease-causing germs (pathogens) like bacteria, viruses, parasites or fungi, and to remove them from the body,  to recognize and neutralize harmful substances from the environment, and to fight disease-causing changes in the body, such as cancer cells.
  • 7. How does the immunity work?  The immunity has a vital role: It protects your body from harmful substances that could make you ill.  It is made up of various organs, cells and proteins.  As long as your immune system is running smoothly, you don’t notice that it’s there. But if it stops working properly – because it’s weak or can't fight particularly aggressive pathogens – you get ill.  Pathogens that your body has never encountered before are also likely to make you ill.  Some pathogens will only make you ill the first time you come into contact with them. These include childhood diseases like chickenpox.
  • 10.  nonspecific immunity  is the natural resistances with which a person is born.  It provides resistances through several physical, chemical and cellular approaches.  Microbes first encounter theepithelial layers, physical barriers that line skin and mucousmembranes.
  • 11.  Subsequent general defenses include secreted chemical signals (cytokines), antimicrobial substances, fever, and phagocytic activity associated with the inflammatory responses.  The phagocytes express cell surface receptors that can bind and respond to common molecular patterns expressed on the surface of invading microbes.  Through these approaches, innate immunity can prevent the colonization, entry and spread of microbes.
  • 12. INNATE IMMUNITY • Recognition of traits shared by broad ranges of pathogens,using a small set ofreceptors • Rapid response ACQUIRED IMMUNITY • Recognition of traits specific to particular pathogens, using avast array of receptors • Slowerresponse Barrierdefenses: Skin Mucous membranes Secretions Internal defenses: Phagocytic cells Antimicrobial proteins Inflammatory response Natural killercells Humoral response: Antibodies defendagainst infection in bodyfluids. Cell-mediated response: Cytotoxic lymphocytes defend against infection in bodycells. Pathogens (microorganisms andviruses)
  • 13. FEATURES  Acts in the minute:- is the 1st line of host defence against infection.  Prior microbial exposure is not required.  Diversity is limited:- it is active only against a limited repertoire of antigen.  Non specific:- it can directed against any microbial antigen, not for particular.  No memory :- it does not have a memory component.  Note :- innate immunity may be considered at the level of the species, races or individual.
  • 14. 1. Species immunity: is the innate immunity towards a microbes exhibited by all members of given species,e.g , frogs are resistant to bacillus anthracis; while towards are susceptible. 2. Racial immunity: some time innate immunity is confined to a particular race; which may be absent in the other communities. E.g. negroes of America are more susceptible to tuberculosis than the white. 3. Individual immunity: it is refer to the antimicrobial defense mechanisms that are confined to a particular individual.
  • 15. FACTORS INFLUENCING INNATE IMMUNITY 1. Age :  In fetus 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.
  • 16.  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
  • 17. MECHANISM OF INNATE IMMUNITY:  1. Epithelial surface:  a. Skin:  It acts as a machanical barrier to microorganisms and provide bactericidal  secretions  Resident microflora of skin and mucous membrane suface help to prevent
  • 18.  colonisation by pathogens  Altertation of normal resident flora may lead to invasion by extraneous microbes and thus causing serious disease. e.g Clostridial enterocoloitis fallowing oral antibiotics
  • 19.  b. Resiratory tract:  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
  • 20.  c. Intestinal tract:  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
  • 21.  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 uretar
  • 22. 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.
  • 23. 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.
  • 24. Phagocytic cells are classified as: i) Microphages e.g. polymorphomucleraleucocytes ( neutrophils) ii) Macrophages e.g mononuclear phagocytic cells
  • 26.  Phagocytic action are divided into 4 stages: i) Chemotaxis:  Phagocytes reach the site of infection attracted by chemotactic substances ii) Attachment:  Infective agent gets attached to phagocytic membrane
  • 27. 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 hydrolytic enzymes of lysosomes  Natural killer cells play a important role in non specific defence against viral infections and tumour.
  • 28. 4. INFLAMMATION:  Inflammation occurs as 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
  • 30. 5. FEVER:  Rise of temperature fallowing infection is a natural defence mechanism.  It destroyes the infecting organisms.  Fewer also stimulates the production of interferon which helps in recovery from viral infection.
  • 31. 2. ACQUIRED IMMUNITY  Acquired immunity is defined as the resistant against the infecting foreign substance that an individual adapts during the course of his life.  Not related to innate immunity
  • 32. FEATURE  Mediators :T cells & B cells it is chief mediators of acquired immunity. And other mediators such as:  Classical complement pathway.  Antigen presenting cells (APC).  Cytokine such as IL2, IL4 & IL5.  Response occurs in day.  Requires prior microbial exposure : it develops only after exposure to the microbes.
  • 33.  It is not present prior to the 1st contact with the microbes.  Specific : highly specific  Memory cells present.  Diversity is wide:  Host cells receptors : it is specific for particular microbial antigen. Example T cells receptors , B cells receptors & immunoglobulin receptors.
  • 35. Active immunity VS. Passive immunity
  • 36. Innate immunity VS. Acquired immunity.
  • 38. ACQUIRED ACTIVE IMMUNITY Resistance developed as a result of antigenic stimulus Also called “Adaptive Immunity Active involvement of host immune apparatus Leads to production of antibodies / Immunologically active cells Takes time to set in after infection
  • 39.  Initial NEGATIVE PHASE : The level of measureable immunity is lower than it was before exposure to antigen. The antigen combines with the existing antibody leading to reduction in existing levels of antibody.
  • 40. Once active immunity sets in It is long lasting One second exposure to same antigen the immune response is quick and abundant Development of humoral & cellular immunity Immunological memory  Active immunization is more effective and confers better protection May be Natural orArtificial
  • 41. NATURALACTIVE IMMUNITY  May be as a result of clinical or inapparentinfection  Measles infection gives the patient life longimmunity  Adults in developing countries have natural active immunity against polio because of inapparent infections inchildhood  Duration of immunity depends on the pathogen  Short term – Eg. Influenza  Long term - Eg. Measeles , chicken pox
  • 42.  Bacterial infections provide with less degree of immunity  PREMUNITION – Seen in syphilis . The immunityto reinfections lasts only till the original infection is active.  Chancroid does not provide the person with any immunity . Person may develop lesionsfollowing reinfection even when original infection isactive.
  • 43. ARTIFICIALACTIVE IMMUNITY • Resistance induced by vaccines • Vaccines are preparations of live or killed microorganisms or their products used for immunization • Bacterial vaccines – Live : BCG vaccine – Killed: Cholera vaccine – Subunit : Typhoid Vi antigen – Bacterial products: Tetanus toxoid
  • 44. • Viral vaccines – Live : OPV-Sabin – Killed : IPV – Salk – Subunit : Hepatitis B Vaccine
  • 45. VACCINES  LIVE VACCINES • Infection without disease • Immunity lasts for several years • Booster doses MAYBE needed • Can be given orally or parenterally  KILLED VACCINES • No infective stage • Less immunogenic • Repeated doses needed – Primary dose – Booster dose • Oral doses not effective • Parenteral doses given with adjuvant to increase humoral immunity
  • 46. PASSIVE IMMUNITY  No infection  Readymade antibodiesare administered  No latent period  No negative phase  Immediate protection  Immunity lasts for short duration till antibodiesare metabolized  No secondary response  Passive immunity decreases with repetition
  • 47. NATURAL PASSIVEACQUIREDIMMUNITY Resistance transferred from mother to baby Via placenta Breast milk – colostrum – IgA IgM production by fetus can start from 20th week of intrauterine life Inadequate immunity at birth By 3 months of age – immunological independence • < 3 months – Pediatric infections are common Active immunization of mother provides passive immunity to infants  Eg. Tetanus toxoid during pregnancy
  • 48. ARTIFICAL PASSIVEACQUIRED IMMUNITY  Resistance transferred by administration of antibodies 1. Hyper immune sera 2. Convalescent sera 3. Pooled human Ɣ globulin  Used for prophylaxis and therapy
  • 49. HYPERIMMUNE SERA • Anti-tetanus serum (ATS) • Prepared from hyperimmunized horses • Temporary protection • Disadvantages • Hypersensitivity • Immune elimination • In use  – Hyperimmune globulin of human origin
  • 50. CONVALESCENT SERA  Sera of patients recovering from disease  Contain high levels of antibody specific to the disease  Use – Viral infections like HepatitisA  Pooled human Ɣ globulin  Ɣ globulin from pooled sera of healthyadults  Has antibodies to all pathogens prevalent in thearea  Use – Rx of patients with immunodeficiencies
  • 51. INDICATIONS FOR PASSIVE IMMUNIZATION • Immediate and temporary protection of a person at risk of developing infection • Toarrest overactive active immunity  Eg. Rh incompatibility
  • 52. Combined immunization  Combination of active and passive methods  Passive immunization for immediate protection  Tetanus  TIG in one arm + TT in other arm  Followed by complete schedule of tetanus vaccination
  • 53. Adoptive immunity  Special type of immunization  Injection of immunologically competent lymphocytes TRANSFER FACTOR  Tried in treatment of Lepromatous Leprosy
  • 54. Local immunity • it is mediated by a type of IgA antibody called secretory IgA which prevent the entry of microbes at the local site itself. • Treatment of infections in a localized area • Polio – – Systemic immunity by IPV • Does not prevent multiplication of virus in thegut – This is achieved by OPV • Influenza – Killed vaccine brings about a humoral response • Not enough to prevent infection • Intra nasal live virus injection/ natural infectionprovides local immunity – IgA
  • 55. Immunoglobulin A (IgA) • Secretory IgA • Produced locally by plasma cells on mucosal surfaces / Secretory glands • With exposure to an antigen Specific IgA is produced • Mucosal defense • Handling of antigens contracted from food and external environment
  • 56. Herd immunity  Overall immunity in a community  Useful in control of epidemics  When LARGE NUMBER of people in a community are immune to a specific pathogen Herd immunity is SATISFACTORY  Eradication of communicable disease lies in development of good herd immunity rather than developing individual immunity
  • 57. How to measurement of immunity  Practically not possible to measure accurately  Simple method is to demonstrate the presence of a specific antibody – Not reliable as one pathogen will illicit immune response to multiple antigens  Antibody demonstration – Agglutination – Precipitation – Complement fixation
  • 58. CONTI….. – Hemagglutination inhibition – Neutralization – ELISA  If antigenic component is identified in-vitro or in-vivo assays can be done. If immunity is associated with cell mediated immunity – Skin tests for delayed hypersensitivity – In-vitro tests for Cell mediatedimmunity
  • 59. 1.MCQ 1.Which of the following statement is false about active immunity? a) Immunological memory is present b) Produced by host immune system c) Immunity develops immediately d) It is effective only after short period 2. Memory cells present in(…..) a) Active immunity b) Passive immunity c) Both d) Non of these
  • 60. 3. Innate immunity contain all cells except: a) N. K cells. b) Dendritic cells c) Mast cells d) B cells 4. Example of killed vaccine? a) BCG b) Typhoid Vi antigen c) Cholera vaccine d) Non of these
  • 61. 5. Which type of antibody found in breast milk? a) IgM b) IgG c) IgA d) IgE 6. N. K cells component of: a) Innate immunity b) Acquired immunity c) Active immunity d) Passive immunity
  • 62. 7. Phagocytic cell is component of: a) Adaptive immunity b) Innate immunity c) Both d) Non of these 8. Which of the following about passive immunity is true? a) Memory cells present b) Memory cells absent c) It produced due to contact with antigen d) More effective in protection
  • 63. 2.WRITE A SHORT NOTE : 1. What is Immunity? Briefly describe acquired immunity. 2. Herd immunity. 3. Acquired immunity. THANK YOU!