Immunity by Dr. Rakesh Prasad Sah

1. IMMUNITY
By Dr. Rakesh Prasad Sah
Assistant Professor, Microbiology

2. The Perfect World

3. The Perfect World

4. CONTENT
Definition.
Classification of immunity.
Innate immunity.
Types of Innate immunity.
Host factor in innate immunity.
Mechanism of innate immunity.
Acquired immunity.
Types of acquired immunity.
Local immunity.
Herd immunity

5. What is immunity?
 Resistance shown by host to microorganisms. It
also includes resistance to toxic molecules or
foreign cells.
 The immune system produces antibodies or
cells that can deactivate pathogens.
 Fungi, protozoan's, bacteria, and viruses are all
potential pathogens.

6. CLASSIFICATION
INNATE IMMUNITY
(Present Since
Birth)
AQUIRED IMMUNITY
(After Birth Specific immunity to
a Particular Pathogens)
ACTIVE IMMUNITY PASSIVE IMMUNITY
NATURAL
ARTIFICIAL NATURAL ARTIFICIAL

7. Innate (Nonspecific) Immunity
It is also called native immunity.
Present naturally since birth.
It is non specific in nature.
This type of immunity persist for life.
Types:
Species immunity
Racial immunity
Individual immunity

8. Species immunity:
• Species show variation in their resistance.
• Man is resistance to many plant pathogens.
• Birds are resistance to tetanus.
(Reason: Physiological & Biochemical difference
between tissues of different species- determine whether
pathogen will multiply or not. )
Racial Immunity:
Within in species different races show different
resistance….
• Algerian Sheep – resistance to anthrax, other races –
suspected.
• Tuberculosis is more common in Negros than
American's.

9. Individuals Immunity:
Different individuals have different
susceptibility or resistance.
Ex. In a group of person exposed to a
pathogens- some person will develop the
disease- severe/moderate/mild type
where as some will have asymptomatic
infection.

10. Host factor in innate immunity
 Age: High susceptibility at extremes age.
• Foetus /neonate – immature immune system
• Old person - decrease of immune response.
 Hormonal influence
• Diabetes mellitus (elevated level of carbohydrate in tissue)
• Hypothyroidism
• Adrenal dysfunction(increased corticosteroid secretion)
 Malnutrition.

11. Mechanism of innate immunity
(Natural Resistance)
 A.Epithelial surfaces
 B.Antibacterial substances in blood & tissues
 C.Microbial antagonism
 D.Cellular factors
 E.Temperature
 F.Inflammatory process
 G.Acute phase proteins

12. A. Epithelial Surfaces
1. Skin & mucous membrane - protect against
invasion by microbes.
Healthy skin –
- high salt conc. in sweat
- sebaceous secretions
- long chain fatty acids & soaps
-

13. A. Epithelial Surfaces
 Respiratory tract - nose architecture
- cough reflex
- mucosal secretions
- phagocytes in alveoli

14. A. Epithelial Surfaces
2. Saliva - inhibits many micro-organisms.
3. Gastric acidity –
destroys many microbes.
4. Intestinal mucosa - mucus , peristalsis

15. A. Epithelial Surfaces
5. Conjunctiva - flushing action of lachrymal
secretions (tears - contains lysozymes)
Lysozymes:
◦ antibacterial substance
◦ present in tissue fluid & all secretions
◦ except CSF, urine & sweat
◦ also present in phagocytes
6. Flushing action of urine
7. Acidic pH of adult vagina
8. Spermine & zinc in semen is antibacterial

16. B. Antibacterial substances in
blood & tissues
1.Complement system
2.Basic polypeptides – like leukins derived from
leucocytes & platelets
3.Lactic acid in muscle
4.Lactoperoxidase in milk.
5.Interferons - antiviral

17. C. Microbial antagonism
1.resident flora on skin & mucosa prevent
colonisation by pathogens.
2.altered flora following oral antibiotics may lead
to enterocolitis.

18. D. Cellular factors
1.Phagocytic cells
2.Natural killer cells
3.Eosinophils

19. 1. Phagocytic Cells
 Phagocytic cells : 2 types - polymorphonuclear
leucocytes - mononuclear phagocytes:
in blood & tissues
Monocytes macrophages
Imp. link between innate & acquired immunity
Chemotaxis - phagocytes are attracted to the site
of infection by chemotactic factors.

20. Phagocytosis
 Involve –
◦ recognition & binding
◦ ingestion and
◦ Digestion
◦
 Requires opsonins - molecules on the surface of
certain bacteria which bind to the receptor on
phagocytes - Opsonization.

21. Phagocytic action

22. 2. Natural killer cells
 Class of lymphocytes important in non-specific
defense against viral infections & tumor cells.
 Activated by interferons & selectively kills viral
infected cells & tumor cells.

23. 3.Eosinophils
 Number increases during parasitic infections &
allergic conditions.
 Not efficient phagocytes but their granules
contain molecules that are toxic to parasites.

24. E. Temperature
1.Many micro- organisms are temperature
dependent e.g. tubercle bacilli, pathogenic to
mammals, do not infect cold-blooded animals.
2.destroys infecting pathogen
e.g. fever induction used to destroy T. pallidum
before Pn became available for treatment.

25. F. Inflammation
1.Non specific defense mechanism.
2.Follows tissue injury or irritation caused by the
entry of pathogens or other irritants
3.Events that occur are
– Vasodilatation
- Increased vascular permeability &
- Cellular infiltration
4.Changes are brought about by chemical
mediators like histamine, PGs, LTs.
5.Signs : redness, heat, swelling & pain.

26. G. Acute phase proteins
1.Present in normal serum at very low levels but
their concentration rises dramatically during an
infection e.g. C-reactive protein (CRP)
2.Enhance host resistance, prevent tissue injury &
promote repair of inflammatory lesions.

27. Acquired Immunity
“Resistance acquired by an individual during life”
1. Active immunity
2. Passive immunity

28. Active immunity
Induced in an individual after effective contact with an
antigen.
Follow either natural infection or vaccination.
Actively participates in producing antibody .
Often cell- mediated immunity also.
Develop slowly over a period of days or weeks of
time, usually for year.

29. Mechanism of development of active immunity

30. Antibody response to pathogens/ vaccines:
Primary antibody response – on first contact with pathogen /
vaccine
Secondary antibody response- on further contact with pathogens/
vaccine.
ANTIBODY RESPONSE TO PATHOGEN / VACCINES
10 20 35 40 50 60 (DAYS)
ANTIBODYLEVEL

31. Primary response:
Lag phase :
After entry of pathogen or vaccine, some time (5-6 days) are
required for sensitization of immune apparatus.
Log Phase:
Antibody appears in blood and increases in titer (level).
Plateau:
Antibody formation and catabolism is almost equal.
Phase of decline:
Catabolism exceeds the antibody formation, hence there is
decrease in Ab level.

32. Secondary Responses:
Memory cells, which are produced in primary responses,
react to further contacts with pathogen/ vaccines quickly and
produce the antibodies in very short time. There is no lag
phase, and antibodies levels rises quickly.
Types of antibodies produced:
Initially IgM type of antibodies are produced followed by IgG
type. IgM antibodies persist for shorter period, while IgG
antibodiues persist for longer period.

33. Natural active immunity
Acquired by natural infection by the microorganism by sub
clinical infection.
Play important role in preventing epidemic.
Eg. Smallpox

34. Artificial active immunity
Resistance produced by vaccination.
Vaccination: A vaccination is an injection of a weakened form of the actual antigen
that causes the disease. The injection is too weak to make you sick, but your B
lymphocytes will recognize the antigen and react as if it were the "real thing". Thus,
you produce MEMORY cells for long term immunity.
Bacterial vaccines
Live: BCG, anthrax, plague & brucella.
Killed: TAB for enteric fiver
Viral vaccines:
Live: small pox, measles, influenza, mumps, sabian
Killed: salk

35. Passive immunity
Resistance is induced by transfer of preformed
antibodies against infective agent or toxin in another host.
Immune system play no active role and the protective
mechanism comes into force immediately after transfer of
antibodies (immune serum).
Types:
Natural passive immunity
Artificial passive immunity

36. Natural passive immunity
A mother will pass immunities on to her baby during
pregnancy - through transplacentally.
Mother milk (colostrums) contain maternal antibodies
will protect the baby for a short period of time
following birth while its immune systems develops.

37. Artificial passive immunity
Resistance passively transferred to a recipient by the
administration of antibodies.
Antisera produce in animals-
Horses/ Sheep are given increasing doses of pathogen/ toxins,
until high level of circulating antibodies are produced.
Animals are bled and serum is separated- called as hyper immune
serum.
Examples- Antisera against tetanus, diphtheria, gas gangrene.
These antisera contain foreign protein and can give rise to
anaphylactic shock, cause death of patient. Hence skin sensitivity
test is necessary before administration of these antisera.

38. Antisera of human origin-
Obtained from convalescent patients who have high antibody
levels for particular pathogen.
Or surgical injections of pathogens are given to human
volunteers. When sufficient antibody levels are achieved ,
blood is obtained and sera separated.
These sera must be tested for antibodies to Hepatitis B
surface antigen, Hepatitis C antigen, HIV infections.
No danger of hypersensitivity reaction with human antisera.
But they are expensive.

40. Local immunity
Proposed by BESREDKA 1919-1924.
Many pathogen have fixed route of entry and multiplication
in particular tissues. Hence vaccines effective at site of entry
& multiplication will be more useful.
Ex. Oral polio vaccine is preferred over salk polio IM vaccine,
influenza vaccine administered intra nasally.

41. Herd immunity
It is the over all immune status of a community and is
important in the control of epidemic outbreaks.
When herd immunity is low, the outbreak of an infectious
disease may be rapid and more severe in nature. It the herd
immunity is high the spread disease is less rapid and is of
mild form.
Developing a high level of herd immunity by means of
active immunization will help in the eradication of
communicable disease in the community.