ACQUIRED IMMUNITY

Most potential pathogens are checked by innate immunity

before they establish an overt infection. If these defences are
breached the acquired immune system is called into play.

The resistance that an individual acquires during his life-time

is known as acquired immunity.

It is antigen-specific and may be antibody-mediated or cell-

mediated.

It is of two types:

Active immunity and

Passive immunity
 ACTIVE IMMUNITY

This involves the active involvement of the person’s own

immune apparatus leading to the synthesis of antibodies and/or
the production of immunocompetent cells (ICCs).

It appears only after a lag (latent) period i.e., the time required for
generation of antibodies and ICCs.

During development of active immunity there is often a negative

phase during which the level of measurable immunity may actually
be lower than before antigenic stimulus. This is due to antigen
combining with pre-existing antibodies and lowering its level.
If an individual who has been actively immunized against an antigen,
experiences the same antigen subsequently, the immune response
occurs more quickly and more abundantly than during the first
encounter. This is known as secondary response.

Immune system is able to retain the memory of a prior antigenic

exposure for long periods and produces a secondary type response
when encountered with the same antigen. This is known as
immunological memory.
 PASSIVE IMMUNITY

The immunity that is transferred to a recipient in a ready-made

form is known as passive immunity.

Here the recipient’s immune system plays no active role.

There is no lag or latent period, the immunity is effective

immediately after passive immunization.

There is no negative phase.

It confers only transient immunity lasting usually for days or weeks

till the antibodies are metabolized and eliminated.

There is no secondary type response.

Subsequent administration of antibodies is less effective due to
immune elimination.

Following first injection of antibody, its elimination is only by

metabolic breakdown but during subsequent injections its
elimination is much quicker because metabolic breakdown is
combined with immune elimination as it combines with
antibodies to horse serum that would have been produced following
first injection.

This happens when horse (foreign) serum is used.

Immune elimination is not a problem when human serum is used.

Because of its immediate action it is employed where instant
immunity is required as in case of protection against tetanus, gas
gangrene and diphtheria following exposure.
Active immunity may be

•Natural or
•Artificial
 NATURAL ACTIVE IMMUNITY

• Natural active immunity results either from a sub-clinical or

clinical infection.

• A large majority of adults in the developing countries possess

natural active immunity to poliomyelitis due to repeated
subclinical infections with poliovirus during childhood.

• Some infections like diphtheria, whooping cough, measles and

mumps induce long-lasting immunity.
Common cold and influenza confer immunity which lasts for a short
time.

In case of influenza, short-lived immunity is due to the ability of

influenza virus to undergo antigenic variation, so that immunity
following first infection is not effective against second infection due
to an antigenically different virus.

In general, immunity following bacterial infections is generally

less permanent than that following viral infections.
In some infections like syphilis and malaria, immunity lasts only till
original infection remains active. This is known as premonition or
infection-immunity. Once the disease is cured the patient becomes
susceptible again.
 ARTIFICIAL ACTIVE IMMUNITY

This is the resistance induced by vaccines which are preparations

of live or killed microorganisms or their products.

V. Bacterial vaccines

(g) Live :

B.C.G. for tuberculosis

Ty 21a for typhoid

(b) Killed :

TAB for enteric fever

Cholera
Pertussis
II. Bacterial products

Tetanus toxoid
Diphtheria toxoid
Capsular polysaccharide of meningococci
Capsular polysaccharide of Haemophilus influenza type b
III. Viral vaccines

(d)Live:

Sabin vaccine for poliomyelitis or oral polio vaccine (OPV).

MMR vaccine for measles, mumps, rubella
Varicella-zoster

(b) Killed :

Salk vaccine for poliomyelitis

Neural and non-neural vaccines for rabies
Influenza
Hepatitis A
Hepatitis B
Japanese encephalitis
Live vaccines initiate a sort of mini infection without causing
disease.

Since live vaccines undergo limited multiplication in the body,

therefore, number of organisms required in a dose is less; single
doses may be sufficient and they are relatively cheaper.

Live vaccines may be administered orally.

Since they are live, therefore, strict conditions of storage are

required.
Killed vaccines are generally less immunogenic than live vaccines
and protection lasts only for a short period. Therefore, they have
to be administered repeatedly.

At least two doses are required.

First dose is known as primary and subsequent doses as booster

doses.

In killed vaccines since the organisms are killed, therefore, larger

number of these are required in each dose. Strict conditions of
storage are not very essential.
Oral route for killed vaccines is generally not effective.

Anti-body response to killed vaccines is improved by addition of

adjuvants
For example, aluminium phosphate adjuvant vaccine for cholera.
 NATURAL PASSIVE IMMUNITY

This is the resistance transferred from mother to foetus through

placenta.

IgG antibodies can cross placental barrier to reach the foetus.

After birth, immunoglobulins are passed to the newborn through

the breast milk.

Human colostrums is rich in IgA antibodies which are resistant to

digestion in stomach and small intestine, hence confers immunity on
the neonate up to three months of age.

Human foetus acquires some ability to synthesize IgM antibodies

from twentieth week of life, but its immunological capacity is still
inadequate at birth.
It is only by the age of three months that the infant acquires a
satisfactory level of immunological independence.

Transport of antibodies across placenta is an active process, therefore

the concentration of antibodies in foetal blood may sometimes be
higher than that seen in the mother.

These antibodies are generally against all common infectious

diseases in the locality.

Therefore, most paediatric infections are common after the age of

three months when maternal immunoglobulins disappear.

By active immunization of mother during pregnancy the immune

status of the neonate can be improved. Therefore, immunization of
pregnant women with tetanus toxoid is recommended in countries
where neonatal tetanus is common.
 ARTIFICIAL PASSIVE IMMUNITY
This is the immunity transferred passively to the recipient by
administration of antibodies.

This is done by administration of hyperimmune sera of man or

animals.

For example, tetanus antitoxin is prepared in horses by active

immunization of horses with tetanus toxoid, bleeding them and
separating the serum.

Similarly, diphtheria antitoxin and gas gangrene antitoxin are also

prepared.
Since these antitoxins are foreign proteins and are liable to cause
serious or even fatal hypersensitivity reactions, these should be
administered only after testing for hypersensitivity.

After first administration, it is removed by metabolism and

following subsequent injections by metabolism and immune
elimination. Therefore, immunity conferred is short-lived.

Sera collected from patients convalescing from infectious

diseases contain high levels of specific antibodies.

Convalescent sera have, therefore, been employed for passive

immunization against viral infections such as measles and rubella.