Download IMMUNITY

IMMUNITY
Babitha Elias
DEFINITION
Immunity refers to the resistance
exhibited by the host towards injury
caused by microorganisms and their
products.
Types of immunity
INNATE IMMUNITY
Definition:
Resistance to infections which an
individual possesses by virtue of his
genetic and constitutional make-up.
 It
is not affected by prior contact with
microorganisms or immunisation.
 It
is non specific.
I. INNATE IMMUNITY
Types of innate immunity

Species

Racial

Individual
Species immunity: total or relative
refractoriness to a pathogen, shown by all
members of a species.
Eg: human spp are resistant to plant
pathogens
Racial immunity: Within a species, different
races may show resistance in susceptibility
to infections.
Eg: Resistance of Algerian sheep to anthrax.
Resistance of Caucasians to Tb
Individual immunity: the differences in
innate immunity exhibited by different
individuals in a race.
Eg: innate immunity in Twins.
FACOTRS THAT INFLUENCE THE
INNATE IMMUNITY
 Age
 Hormones
 Nutrition
AGE
 Extremities of age is susceptible to
infection.
 Fetus in utero – protected by the placental
barrier.
 Congenital malformations can occur if the
pathogens cross the placental barrier –
Eg: Toxoplasma, Rubella,
Cytomegalovirus, Herpes infections.
 Susceptibility
in the young – hormonal
influence.

Eg: Tinea capitis, gonorrhea in prepubertal
girls
 Some
infections are severe in adults due
to hypersensitivity.

Eg: Poliomyelitis, Chickenpox.
 Some
infections are asymptomatic in
newborn – lack of adequate immune
response.

Eg: Hepatitis B
HORMONAL INFLUENCES
 Endocrine disorders like diabetes mellitus,
hypothyroidism, adrenal dysfunction –
increased susceptibility to infection.
 Corticosteroids –


Depress the host’s resistance by antiinflammatory, anti-phagocytic effects,
suppression of Ab formation and by
hypersensitivity.
Elevated steroid level in pregnancy - increase
susceptibility.
NUTRITION
 Malnutrition predisposes to bacterial
infections.
 Some
infections may not become clinically
apparent in severely malnourished.

Eg: malaria.
MECHANISMS OF INNATE IMMUNITY
 Epithelial
surfaces
 Antibacterial substances in blood & tissues
 Cellular factors in innate immunity.
 Inflammation
 Fever
 Acute phase proteins
Epithelial surfaces
 Intact
skin & mucous membrane covering
the body – gives protection against
invasion of microbes.
Skin
 Possesses bactericidal activity.
 Sweat, sebaceous secretions provide
protection.
 Normal flora of skin


Resident flora – group of organisms present on the
skin which are not easily removed by washing and
disinfectants.
Transient flora – bacterial flora which is easily
removed by washing & disinfectants.
 Normal
flora - prevent colonisation by
pathogens.
of normal resident flora – lead to
invasion of microbes
 Alteration

Eg: Staphylococcal or Clostridial enterocolitis
following oral antibiotics.
Respiratory tract:
 Architecture of nose
 Nasal & respiratory secretions
 Ciliary action
 Cough reflex
Intestinal tract:
 Saliva
 Acidity of stomach
 Gastric juices
 Normal flora – prevent colonisation of
pathogens
Conjunctiva:
 Flushing action of tears.
 Lysozyme in the tears.
Genitourinary tract:
 Flushing action of urine.
 Acidic pH of vaginal secretions.
 Spermin from semen.
Antibacterial substances in blood &
tissues
 Complement
 Properdin
 Beta
lysin
 Leukins & plakins
 Lysozyme
 Interferon against viral infections
Cellular factors in innate immunity
cells – microphages &
macrophages
 Natural Killer (NK) cells
 Phagocytic
Phagocytosis
 Metchnikoff (1883)
 Phagocytosis is a process by which the
microorganisms are ingested and
destroyed by the phagocytic cells.
Microphages – polymorphonuclear
leukocytes (Neutrophils)
 Macrophages – histiocytes (tissue) &
monocytes (blood)
Steps in phagocytosis
1. Chemotaxis
2. Adherence
3. Ingestion
4. Intracellular killing

Inflammation
 Tissue
injury or irritation initiated by the
entry of pathogens or other irritants leads
to inflammation.
 Inflammation
leads to vasodilation,
increased vascular permeability, cellular
infiltration.
 Microorganisms
destroyed.
are phagocytosed &
 There
is outpouring of plasma, which
helps to dilute the toxic products present.
A
fibrin barrier is laid.
 Inflammation




Redness
Heat
Swelling
Pain
is characterized by
Fever
 Rise
 It
in temperature following infection.
accelerates the physiological processes.
 Sometimes
 Stimulates
destroy the pathogens.
the production of interferons.
Acute phase proteins
 Infection
or injury leads to sudden
increase in plasma concentrations of
certain proteins – Acute phase proteins.
 They include C reactive protein (CRP),
mannose binding protein.
 They enhance host resistance, activate
alternate pathway of complement, prevent
tissue injury, promote repair of
inflammatory lesions.
ACQUIRED IMMUNITY
DEFINITION
The specific resistance acquired by an
individual during life.
II. TYPES OF ACQUIRED (ADAPTIVE)
IMMUNITY
Natural (clinical/subclinical infection)
a) Active
Artificial (vaccination)
Natural (mother to child)
b) Passive
Artificial (antiserum)
ACTIVE IMMUNITY
DEFINITION: Active immunity is the specific
resistance against an infection which
develops after exposure to immunogen.
 Produced
actively by the immune system.
 Develops after a latent period – required
for the immune system to act.
 Immunity is long lasting.
Mechanism of active immunity
2 Mechanisms:
I.
Humoral immunity
II.
Cell mediated immunity
Humoral immunity (Antibody mediated)

It depends on the synthesis of
Antibodies by plasma cells.

Plasma cells – which produce & secrete
antibodies specifically against the
antigen
The specific antibodies produced provide
resistance by the following mechanism:
 Neutralization
i) Specific Abs produced against toxins are called
antitoxins, which neutralize the toxin & give
protection against toxic bacterial infection.

Eg: Tetanus, Diphtheria
ii) Specific Abs produced against infectious
agents can neutralize a pathogen

Eg: Neutralizing Abs against viruses.
 Opsonisation

Ab produced against an infectious agent
could act as an OPSONIN which can enhance
adherence of infectious agent onto the
phagocyte & enhances phagocytosis.
 Complement

fixation
Ab can activate complement by classic
pathway. After the activation of complement, it
mediate mechanisms such as opsonisation,
chemotaxis & cell lysis.
CELL MEDIATED IMMUNITY (CMI)
 Cell
mediated immune response depends
on T – lymphocytes developed against
certain antigens.
 CMI
gives protection against viral, parasitic,
fungal & intracellular bacterial infections –
tuberculosis, leprosy etc.
TYPES OF ACTIVE IMMUNITY
1.



Natural Active immunity
It is the specific resistance an individual
develops after infection – either clinical or
sub-clinical infection.
Immunity is long lasting. Eg: Chickenpox,
Mumps & measles.
Immunity may be short lived – Eg:
Influenza, common cold
Artificial Active immunity
 It is the specific resistance which
develops in an individual after
vaccination.
 Vaccines – are preparations which
consists of live attenuated or killed
microorganisms or toxoids used for
immunization purposes.
Live attenuated vaccines:
Attenuation : is a process by which the
virulence of an organism is reduced
without altering the immunogenicity.
2.
 Attenuation
is done by growing the
microorganisms at unfavorable conditions.
 Eg:





BCG vaccine for tuberculosis
Ty 21a vaccine for typhoid
Sabin vaccine for poliomyelitis
MMR vaccine for Mumps, measles, rubella
17D vaccine for yellow fever
Killed vaccine
 The organisms are killed by heat, formalin,
phenol & alcohol.
 These are preserved in phenol or alcohol.
 Eg:



TAB vaccine for enteric fever
Salk vaccine for poliomyelitis
Antirabies vaccine
Toxoids:
 Toxoids are inactivated exotoxins which
has lost its toxicity but has retained its
immunogenicity.
 Used to immunize against bacterial
infections – diphtheria & tetanus.
 Eg: DPT vaccine
PASSIVE IMMUNITY
DEFINITION:
Specific resistance which develops in an
individual after receiving preformed
antibodies.
 The antiserum is prepared by injecting
infective agent or toxin in another host.
 Immune system has no active role.
 Protection starts immediately after the
administration of antiserum.
 No
latent period.
 Immunity is short lasting.
TYPES OF PASSIVE IMMUNITY
 Natural
 Artificial
Natural passive immunity
 Specific resistance which a child receives
from mother through placenta or through
milk.
Clinical significance
 Protects the child from many infections

Eg: Rota virus diarrhoea
 Active
immunization of pregnant female
with Tetanus toxoid will immunize the
mother & protects the child from neonatal
tetanus.
Artificial passive immunity
 Develops in an individual following
administration of antisera or immunoglobulin
 The source of the antisera may be animal or
human origin, convalescent sera, pooled
gammaglobulin.
Animal sera
 Prepared by immunizing horse with toxoid.
 Eg:


Anti-tetanus serum (ATS)
Anti-diphtheria serum (ADS)
Disadvantages:
1. As animal sera is foreign protein – causes
hypersensitivity reactions in humans.
of immune elimination – the specific
Abs formed will combine with the antisera
given subsequently & get eliminated
quickly
2. Risk
Human antisera
 Prepared
by hyperimmunisation of human
volunteers with toxoid.
 Protection with human antisera lasts
longer & there is no immune elimination.
Convalescent sera
 Sera of patients recovering from infectious
diseases.
 Eg: Used against Measles & Rubella.
Pooled human gammaglobulin
 Prepared
by using sera of healthy
individuals.
 Eg: For viral hepatitis A
Uses of Passive immunity
1. Provide
immediate short term protection in
a non-immune host.
2. For the suppression of active immunity
which may be injurious – Eg: for Rh
incompatibility
3. For the treatment of serious infections.
Differences between Active & Passive immunity
Features
Contact with
immunogen
Lag period
Active immunity
Passive immunity
Yes
No
Present
Absent
Long lasting
Short
Present
Absent
Negative phase
Present
Absent
Usefulness in
immunodeficient
host
No
Yes
Duration of
protection
Memory
Local immunity
 It
is the resistance an individual has at the
site of entry of pathogen.
 Provided by secretory Ig A.
 Eg: Oral polio vaccine.
Herd immunity
 It
refers to overall resistance in a
community.
 Eg: OPV
 Eradication of any communicable disease
depends on development of high level of
herd immunity