Acquired Immunity

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 cellmediated. 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.