Immunity powerpoint for Second MBBS Undergraduate students

1. IMMUNITY
Dr. SOMESHWARANRAJAMANI,MBBS, MD.,
AssistantProfessor & ClinicalMicrobiologist,
Karpagam Faculty of Medical Sciences and Research,
Othakalmandapam, Coimbatore-641032

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. 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. Types of Immunity
• Immunity against infectious disease is 2 types:
1. Innate or Native immunity
2. Adaptive or Acquired immunity

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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. Innate immunity Vs Adaptive immunity

19. Innate immunity Vs Adaptive immunity

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

22. Types of Adaptive immunity
• Active immunity
• Passive immunity

23. 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

24. 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

25. 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)

26. 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.

27. 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.

28. Types of Passive immunity
• Natural passive immunity
• Artificial passive immunity
• Combined immunisation

29. 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.

30. 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.

31. 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.

32. 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.

33. 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.

34. 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

35. 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.

36. 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

37. 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.

38. Herd immunity
Herd- Large proportion of individuals in a community
Infectious pathogen causing communicable disease
Potential to cause epidemic in susceptible individuals

39. 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

40. SUMMARY & TAKE HOME MESSAGE

41. THANK YOU