The document defines and compares innate, acquired, active, and passive immunity. It describes the mechanisms of innate immunity like epithelial surfaces and cellular factors. It also explains the types of acquired immunity including natural and artificial active immunity induced by infection or vaccination, as well as natural and artificial passive immunity from maternal antibody transfer or administration of antibodies.

1. DR ARUNA RANI BEHERA
ASSISTANT PROFESSOR
DEPARTMENT OF MICROBIOLOGY

2. DEFINITION OF IMMUNITY
 Resistance exhibited by the host towards injury
caused by microorganisms and their products .
 Imp. for prevention of infectious diseases.

4. INNATE IMMUNITY
 Resistance which individual possess from birth by
virtue of genetic & constitutional makeup
 Not depend on prior contact with foreign antigen
Types
1.Nonspecific- resistance to infections in general
Specific- resistance to specific pathogen
2.Species immunity
Racial immunity
Individual immunity

5. Type of
innate
immunity
Explanation Examples
Species
immunity
Innate immunity towards
a microbe exhibited by all
members of a given
species
frogs are resistant to
Bacillus anthracis;
while toads are
susceptible.
Racial
immunity
innate immunity
confined to a particular
race; may be absent in
other communities
Negroes of America are
more susceptible to
tuberculosis than the
whites.
Individual
immunity
Antimicrobial defense
mechanisms that are
confined to a particular
individual; may not be
exhibited by others.
One exception is
identical twins who
exhibit similar degrees
of susceptibility to
infections

6. SPECIES IMMUNITY
 Resistance to infections by
all members of a particular
species.
 Eg; B.anthracis infect
human beings but not
chickens
 Physiological & biological
differences between tissues
of different host species is
responsible.

7. RACIAL IMMUNITY
 With in a species , different
races may show difference in
susceptibility or resistance to
infection
 Algerian sheep
- resistant to anthrax
- Genetic origin
 American negroes are more
susceptible to TB than white
race.

8. African people are resistant to p.falciparum –
Due to sickle cell anemia (heridatary abnormality of red cells )(sickling)

9. INDIVIDUAL IMMUNITY
 Varies with different individual of same race & species.
 Homozygous twins exhibit similar degree of resistance or
susceptibility to LL,TB but not in Heterozygous twins.

10. Factors influencing innate immunity
 Age
 Hormonal influences and sex
 Nutritional factors

11. Age
 The 2 extremes of life( fetus
& old age)-higher
susceptibility to various
infections.
 In fetus-immune system is
immature
 Old persons-gradual waning
of immune response
The foetus in utero
- normally Protected from
maternal infections by
placental barrier.

12. Some pathogens cross this barrier causing Infections
resulting in foetal death.
such as Toxoplasma gondii
Others-
Rubella,
Cytomegalovirus ,
Herpes.
( TORCH )
Due to immaturity of immune system

13. Hormonal influence
 Endocrine disorders such as diabetes mellitus,
hypothyroidism, adrenal dysfunction are associated
with enhanced susceptibility to infection.
 Staphylococcal sepsis is more common in diabetes
 Corticosteroids depress host resistance by anti-
inflammatory , antiphagocytic effects & by inhibiting
antibody formation.
 Pregnancy ,stress ---elevated steroids—higher
susceptibility to infections.

14. Nutrition
 Malnutrition predisposes to
bacterial infections.
 Both humoral & cellular
immunity reduced.
 Malnutrition commonest
cause of immunodificiency.

15. Mechanisms of innate immunity
 Epithelial surfaces
Skin
Respiratory tract ,
Intestinal tract
Conjunctiva
Genitourinary tract
 Antibacterial substances in blood and tissues
 Microbial antagonism
 Cellular factors
 Acute phase proteins
 Inflammation
 fever

16. Epithelial surfaces
 Skin possesses bactericidal activity
 High concentration of salt in drying sweat, sebaceous secretions and
long chain fatty acids
 Skin may be freed of transient flora but not resident flora
 The skin and mucous surfaces have resident flora which prevents
colonisation of pathogen
 Alteration of normal flora –invasion of microbes-serious diseases
 staphylococcal or clostridial enterocolitis following oral antibiotics.

17.  Mucosa of respiratory tract - nose prevents entry
of microorganisms, inhaled particles arrested at
nasal orifices.
 Mucus secretions act as trapping mechanism &
hair like cilia propels the particles towards
pharynx –swallowed or coughed .
 Cough reflex— defense mechanism of the
respiratory tract.
 Phagocytic particles –particles which reach the
Pulmonary alveoli are ingested by phagocytic cells

18. Intestinal tract
 Mouth is constantly bathed in saliva which has
inhibitory effect on microorganisms
 Acidity of stomach destroys microorganisms
 Normal intestinal flora prevent colonisation of
pathogenic bacteria

19. Conjunctiva
 Conjunctiva is freed of foreign particles by the
flushing action of lacrymal secretions.
 The eyes become susceptible to infection when
lachrymal secretions are absent.
 Tears contain the antibacterial substance lysozyme
 Lysozyme
- present in tissue fluids
-absent CSF, sweat , urine.

20. Genitourinary tract
 Urine - eliminates bacteria from the urethra by its
flushing action
 Semen – spermine & zinc present in semen have
antibacterial activity.
 Vagina – acidic pH of vagina due to fermentation
of glycogen in the epithelial cells by lactobacilli
makes it inhospitable to many pathogens.

21. Mechanical barriers and surface secretions

22. Antibacterial substances
 Complement system,properdin , lysozyme
 Complement system plays an Important role in
destruction of pathogenic bacteria (that invade blood
and tissues)
 Betalysin, Leukins from leucocytes , plakins from
platelets
 Interferons-Stimulated by live or killed Viruses.
-Gives protection from viral infections.

23. Cellular factors
 Natural defense against the invasion of blood and
tissues by microorganisms and other foreign particles
is mediated by phagocytic cells.
 Phagocytic cells
Microphages -- polymorphonuclear
leucocytes(neutrophils)
Macrophages- mononuclear phagocytic cells
histiocytes(tissues), reticuloendothelial cells,
 monocytes in blood.
 Natural killer cells (NK cells)

24. Inflammation
 Non specific defense mechanism.
 Tissue injury or irritation initiated by the entry of
pathogens or other irritants leads to inflammation.
 Inflammation-l/t
Vasodilation-the arterioles at the site constrict
initially and then dilate leading to increased blood
flow.
Increased vascular permeability-Out pouring of
plasma- helps in diluting toxic products
Cellular infiltration

25. Fever
 Rise in temperature following
infection is a natural defense
mechanism.
 It destroys the infecting pathogens
 Therapeutic induction of fever
TREPONEMA PALLIDUM in tissues
of syphilitic patients before penicillin
became available.
 Fever stimulates the production of
interferon.

26. ACUTE PHASE PROTEINS
 Infection and injury leads to a sudden increase in
plasma concentration of certain proteins APP.
 C reactive protein,
 Mannose binding protein(MBP)
 Alpha - 1- acid glycoprotein,
 Serum amyloid p component.
 CRP - activate alternate pathway of complement.
 Enhance host resistance, prevent tissue injury and
promote repair of inflammatory lesions

27. Acquired immunity
The resistance that an individual acquires
during life is known as acquired immunity.
2 types.
-Active
-passive.

28. Active immunity Passive immunity
1. Produced actively by host’s
immune system.
2. Induced by infection or by
immunogen
3. Long lasting & effective
protection.
4. Immunity effective only after
lag period.
5. Immunological memory
present.
Booster effect on subsequent
dose.
6. Negative phase may occur.
7. Not applicable in the
immunodeficient
1. Received passively by host,No
active host participation.
2. Ready made antibody
transferred
3. Short lived protection
4. Immediate immunity
5. No Immunological memory
No Booster effect on
subsequent dose.
6. No Negative phase
7. Applicable in the
immunodeficient

29. Active immunity Passive immunity
Produced actively by host
immune system
Immunoglobulins received passively
Induced by
 Infection (natural)
 Vaccination (artificial)
Acquired by-
 Mother to fetus IgG transfer
(natural)
 Readymade antibody transfer
(artificial)
Long lasting Lasts for short time
Lag period present No Lag period
Memory present No Memory
Booster doses-useful Subsequent doses-Less effective
Negative phase may occur No Negative phase
In immunodeficiency
individuals not useful
Useful in immunodeficient
individuals

31. Natural active
immunity
Artificial active
immunity
 Natural active
immunity results from
either a clinical or an
inapparent infection by
a microbe.
 A person who has
recovered from an
attack of Measles
develops natural active
immunity.
poliomylitis, chicken
pox
 Artificial active immunity
is the resistance Induced
by vaccines
 vaccines are preparations
of live or killed
microorganisms or their
products
 Used for immunisation.

32. VACCINES
 LIVE VACCINES
BCG vaccine for tuberculosis
sabin vaccine for poliomyelitis (OPV)
MMR vaccine
Killed vaccine (cholera vaccine)
Ty 21a for typhoid
 KILLED VACCINES
TAB vaccine for enteric fever
salk vaccine for poliomyelitis(IPV)
Killed cholera vaccine
neural & nonneural vaccine for rabies
Subunit (hepatitis B vaccine)
 BACTERIAL PRODUCTS
Tetanus toxoid

33. Natural passive immunity
 Natural passive immunity is the resistance passively
transferred from mother to baby
 In human infants maternal antibodies are transimitted
predominantly through the placenta.
 Human colostrum is rich in IgA antibodies.
 Gives potection to neonate.
 Most paediatric infections common after the age of
3 months

34. Artificial passive immunity
 Resistance passively transferred to a recipient by the
administration of antibodies.
 The agents used for this purpose are hyperimmune sera
of animal or human origin,
 Convalescent sera and pooled human gammaglobulin.
 These are used for prophylaxis, and therapy.

35. MISCELLANEOUS
A.COMBINED IMMUNISATION
active & passive immunisation
B.ADOPTIVE IMMUNITY
injection of immunologically competent lymphocytes
C.LOCAL IMMUNITY
immunity at the site of entry
D. HERD IMMUNITY

36. Herd immunity
 Herd immunity is defined as the overall immunity of a
community (or herd) towards a pathogen.
 Elements that contribute to create a strong herd immunity
are-
o Occurrence of clinical and subclinical cases in the herd
o On-going immunization programme
o Herd structure i.e. type of population involved
o Type of pathogen-Herd immunity may not be strong in a
community against all the pathogens.

37.  Herd immunity develops following effective vaccination
against some diseases like:
o Diphtheria and Pertussis vaccine
o Measles, Mumps and Rubella (MMR) vaccine
o Polio (Oral polio vaccine)
o Smallpox vaccine

38. Q/A
 DIFFERENCE B/W ACTIVE & PASSIVE IMMUNITY
 DIFFERENCE B/W INNATE & ACQUIRED IMMUNITY
 CLINICAL INFECTION LEAD TO—
NATURAL/ARTIFICIAL
 VACCINATION INDUCES-
NATURAL/ARTIFICIAL,ACTIVE/PASSIVE
 ARTIFICIAL PASSIVE IMMUNITY INDUCED BY-
 LIVE VACCINE –
 KILLED VACCINE-