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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.

8. CLASSIFICATION

9. 1. INNATE IMMUNITY

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.
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