Passive immunity is the resistance to infection conferred by transferring pre-formed antibody from an outside source into an individual, rather than by stimulating that individual’s own immune system to produce antibody — the recipient’s own immune system plays no active role in generating the protective antibody.
Key characteristics: acts immediately (no lag period is needed, unlike active immunity, which requires time for clonal expansion), but the protection is short-lived, since the transferred antibody is progressively catabolised over weeks and, because no antigen-specific memory cells are generated in the recipient, the protection does not improve or persist on subsequent exposure.
Types:
Natural passive immunity — transfer of maternal IgG antibody across the placenta to the fetus (providing protection to the neonate during the first few months of life), and transfer of secretory IgA via colostrum/breast milk to the breastfed infant.
Artificial passive immunity — deliberate administration of pre-formed antibody preparations, e.g., immunoglobulin/antitoxin injections — human tetanus immunoglobulin (HTIG), diphtheria antitoxin, rabies immunoglobulin, hepatitis B immunoglobulin, and pooled human immunoglobulin (used for post-exposure prophylaxis or in immunodeficient patients).
Clinical use: valuable when immediate protection is required (e.g., after a high-risk exposure — animal bite for rabies, contaminated wound for tetanus) and there is insufficient time for active immunization to develop protective immunity, or when the individual is unable to mount an adequate active response (e.g., immunodeficiency).
